c

14.03 Dt Trening: Barki: Wyciskanie żołnierskie - 8x 45, 8x 45, 6x 45, 6x 45, 5x 45 Unoszenia sztangi do brody - 10 x40, 10x 40, 8x 40 Unoszenia do przodu - 10x 13, 8x 13, 8x 13 Arnoldki - 12x 13, 10x 13, 10x 13 Wyciskanie sztangi na barki - 70x 5, 30x Triceps: Wyciskanie wąsko - 8x 70, 7x 72,5, 6x 72,5, 6x 72,5, 6x 70 Unoszenia łamaną za głowy - 10x 27,5, 8x 27,5, 6x 27,5 Dipsy - 3x max Francuz hantlami - 12x 10, 12x 10, 12x 10, Wyciskanie wąsko - 100x 20 Suplementacja: Rano: wit a-z 1x, wit. c 0,5g Przed treningiem: beta al 3g, crea 5g, daa 2g Na treningu: bcaa 20g, Po treningu: wpc 30g, beta al. 1g, leucyna 2g, tauryna 1,5 g, crea 5g Na noc: daa 2g, wit a-z 1x, wit. c 0,5g, Zmb 1x Dieta: /SFD/Images/2016/3/18/89f6ec03ddf2447798626b179bab7697.jpg /SFD/Images/2016/3/18/e4715c5bad1548c0a3d795dbc7a9d028.jpg

16.03 Dt Trening.., później szybka szama i do Krakowa do siory.., na miejscu kilka browarków ze szwagrem%-) i zerwana noc.., w poniedziałek też mi się taka trasa szykuję.. Byłem w drodze powrotnej w macu ale tylko na czarnej kawie..., może i bym coś opędzlował ale były 3 autokary dzieciarni i nie chciało mi się stać w kolejce....... Trening: Klatka: Wyciskanie sztangi - 8x 80, 8x 82,5, 7x 82,5, 6x82,5, 6x 80 Wyciskanie sztangielek skos dod. - 10x25, 8x25, 5x25 Rozpiętki - 8x20, 7x20, 6x20 Wyciskanie sztangielek z supinacją - 10x20, 10x20, 8x 20 Wyciskanie sztangi - 100x 20 Biceps: Uginanie ramion sztangą prostą - 8x 40, 8x 42,5, 7x 42,5, 6x 42,5, 5x 42,5 Uginania młotkowe - 10x15, 7x15, 6x15 Modlitewnik - 10x25, 9x25, 8x 25 Uginanie sztangielkami na ławcę skos dod. - 12x 13, 8x13, 7x13 Uginanie ramion sztangą prostą - 100x 5 Suplementacja: Rano: wit a-z 1x, wit. c 0,5g Przed treningiem: beta al 3g, crea 5g, daa 2g Na treningu: bcaa 20g, Po treningu: wpc 30g, beta al. 1g, leucyna 2g, tauryna 1,5 g, crea 5g Na noc: daa 2g, wit a-z 1x, wit. c 0,5g, Zmb 1x Dieta: Szama potreningowa tylko... na miejscu makaron z kurakiem i pesto jeszcze wpadł... /SFD/Images/2016/3/18/74e0bfc032484154b51fd42f51fb053d.jpg /SFD/Images/2016/3/18/a35f079a9753479682cf5a7ad47ca6e9.jpg

19.03 Dt Małżonka upiekła sernik taki normalny nie dietetyczny tzn. z cukrem, ale ograniczyliśmy tłuszcze do minimum i wyszedł trochę suchy.., Dziabałem z sokiem malinowym i było ok...., Trochę mi się te tłuszcze dziś rozjechały i wpadło znacznie więcej..@@-) Ale jakoś zbytnio się nie przejmuję.......... Trening: Nogi: Przysiad - 8x80, 8x85, 7x90, 6x 90, 4x 90 Wykroki ze sztangielkami chodzone - 10x 36, 10x 36, 8x 36 L P Martwy ciąg na prostych nogach - 8x 95, 7x 100, 5x 100 Przysiad bułgarski - 3x10x10 L P Przysiad głęboki - 100x Wspięcia - 24x 80, 18x 90, 16x 90 Suplementacja: Rano: wit a-z 1x, wit. c 0,5g Przed treningiem: beta al 2g, crea 5g, daa 2g Na treningu: bcaa 15g, Po treningu: wpc 30g, beta al. 2g, leucyna 2g, tauryna 1,5 g, crea 5g Na noc: daa 2g, wit a-z 1x, wit. c 0,5g, Zmb 1x Dieta: /SFD/Images/2016/3/20/6931ab1403c54b49868ced4670dc8f94.jpg /SFD/Images/2016/3/20/7591791135994e64af91474515cf59af.jpg

05.04 Dt W tym tygodniu tylko podstawowe ćwiczenia 5x5, bez wcześniejszych serii rozgrzewkowych.... Trening bardzo szybko 45 min.. Po tygodniu laby i tak to poczuję zapewne..:-) Trening: Push: Wyciskanie na płaskiej - 5x 80, 85, 82,5, 80, 80 Wyciskanie żołnierskie - 5x 45, 45, 47,5, 45, 45 Wyciskanie wąsko - 5x 80, 75, 75, 75, 75 Brzuch kółko 3 max Suplementacja: Rano: wit a-z 1x, wit. c 0,5g Przed treningiem: beta al 2g, crea 5g Na treningu: bcaa 15g, Po treningu: wpc 30g, beta al. 2g, leucyna 2g, tauryna 1,5 g, crea 5g Na noc: wit a-z 1x, wit. c 0,5g, Zmb 1x Dieta: /SFD/Images/2016/4/7/e2d6229acde4495994cb76697a0d8dcf.jpg /SFD/Images/2016/4/7/8d07a3f2083848919a306118ffdc3721.jpg

21.06 Dt Trening: BARKI 1. Wyciskanie za głowy siedząc 4x8-10 2. Arnoldki 4x8-10 3. Podciąganie sztangi do brody szerszym chwytem 4x8-10 4. Wznosy sztangielek na boki 7x8-12 (45 sec. rest.) 5. Unoszenia sztangielki w opadzie tylny akton 4x8-12 10 min interwały+kółko 4x Suplementacja: Rano: wit c 2g Przed treningiem: tauryna 1g, AAkg 5g, bcaa 5g, yoha 20 mg Na treningu: bcaa 10g, Po treningu: wpc 30g, leucyna 2g, wit-min 1x Na noc: wit c 2g, omega 3 2x Dieta: Na foto pierwszy i ostatni rozsądny posiłek zaraz po treningu.., Potem w towarzystwie zdjęć nie robiłem.. Resztę potraktujmy jako Cheat meal i tak miał wpaść w tym tygodniu:-D... /SFD/Images/2016/6/22/5724e87066714b1a9bc6b08ff1a8479d.jpg /SFD/Images/2016/6/22/6ad39899c2cb40d5b90d31dd68b07c7e.jpg W realu podliczając napoje chłodzące:-) wpadło jakieś 5 000 kcal.. Zmieniony przez - Leon_ee w dniu 2016-06-22 15:25:05

03/04.06 Dt/Dnt Siema, weekend bardzo fajnie minął, na spontanie wycieczka do Szczawnicy i zaliczenie Palenicy z małą na rękach to był nie lada wyczyn. Podejście to pionówa w zasadzie od początku do końca. Łydki mi tak spinało, że co parę kroków musiałem się zatrzymywać ale to przy ostatnich wzniesieniach. Także miska taka jak w dzień treningowy wyskoczyła głównie za sprawą paru piwek wypitych na miejscu:-) No i szamy w knajpie.., niestety nie nadaje się na jedzenie w takich miejscach, kuchnia niby polska i jak przystało tłusta po prostu, potrawy nawet pierogi muszą w nim pływać:'-( Ale cały czas w ruchu, nie jakieś siedzenie na dupsku, więc myślę, że wszystko spalone.., 03.06 Trening: /SFD/2017/6/5/b02e5ff6099f4a7289a3e392c07bb5ed.jpg Dieta: 2 761,5 kcal 182,0 g 310,3 g 68,4 g /SFD/2017/6/5/1263f44719aa473eac1c75111b798cb0.jpg Suple: wit-min 1x, wit c 1g, omega3 3x, bcaa 12g, beta ala 4g, crea 6g, magnez 300mg, cynk 10mg, czosnek 2x 04.06 Dieta: 2 677,0 kcal 183,6 g 215,3 g 61,0 g /SFD/2017/6/5/2c71d9556c6b4845a45e3f7a02cff402.jpg Suple: wit-min 1x, wit c 1g, omega3 3x, magnez 300mg, cynk 10mg, czosnek 3x Zmieniony przez - Leon_ee w dniu 2017-06-05 09:15:00

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The effects of high-dose glutamine ingestion on weightlifting performance Antonio J, Sanders MS, Kalman D, Woodgate D, Street C. Sports Science Laboratory, University of Delaware, Newark, Delaware 19716, USA. The purpose of this study was to determine if high-dose glutamine ingestion affected weightlifting performance. In a double-blind, placebo-controlled, crossover study, 6 resistance-trained men (mean +/- SE: age, 21.5 +/- 0.3 years; weight, 76.5 +/- 2.8 kg(-1)) performed weightlifting exercises after the ingestion of glutamine or glycine (0.3 g x kg(-1)) mixed with calorie-free fruit juice or placebo (calorie-free fruit juice only). Each subject underwent each of the 3 treatments in a randomized order. One hour after ingestion, subjects performed 4 total sets of exercise to momentary muscular failure (2 sets of leg presses at 200% of body weight, 2 sets of bench presses at 100% of body weight). There were no differences in the average number of maximal repetitions performed in the leg press or bench press exercises among the 3 groups. These data indicate that the short-term ingestion of glutamine does not enhance weightlifting performance in resistance-trained men. The effect of free glutamine and peptide ingestion on the rate of muscle glycogen resynthesis in man. van Hall G, Saris WH, van de Schoor PA, Wagenmakers AJ. Department of Human Biology, Maastricht University, The Netherlands. RH01769@RH.DK The present study investigated previous claims that ingestion of glutamine and of protein-carbohydrate mixtures may increase the rate of glycogen resynthesis following intense exercise. Eight trained subjects were studied during 3 h of recovery while consuming one of four drinks in random order. Drinks were ingested in three 500 ml boluses, immediately after exercise and then after 1 and 2 h of recovery. Each bolus of the control drink contained 0.8 g x kg(-1) body weight of glucose. The other drinks contained the same amount of glucose and 0.3 g x kg(-1) body weight of 1) glutamine, 2) a wheat hydrolysate (26% glutamine) and 3) a whey hydrolysate (6.6% glutamine). Plasma glutamine, decreased by approximately 20% during recovery with ingestion of the control drink, no changes with ingestion of the protein hydrolysates drinks, and a 2-fold increase with ingestion of the free glutamine drinks. The rate of glycogen resynthesis was not significantly different in the four tests: 28 +/- 5, 26 +/- 6, 33 +/- 4, and 34 +/- 3 mmol glucosyl units x kg(-1) dry weight muscle x h(-1) for the control, glutamine, wheat- and whey hydrolysate ingestion, respectively. It is concluded that ingestion of a glutamine/carbohydrate mixture does not increase the rate of glycogen resynthesis in muscle. Glycogen resynthesis rates were higher, although not statistically significant, after ingestion of the drink containing the wheat (21 +/- 8%) and whey protein hydrolysate (20 +/- 6%) compared to ingestion of the control and free glutamine drinks, implying that further research is needed on the potential protein effect. Exercise-induced immunodepression- plasma glutamine is not the link. Hiscock N, Pedersen BK. Copenhagen Muscle Research Centre and Department of Infectious Diseases, Rigshospitalet, University of Copenhagen, DK-2100 Copenhagen, Denmark. The amino acid glutamine is known to be important for the function of some immune cells in vitro. It has been proposed that the decrease in plasma glutamine concentration in relation to catabolic conditions, including prolonged, exhaustive exercise, results in a lack of glutamine for these cells and may be responsible for the transient immunodepression commonly observed after acute, exhaustive exercise. It has been unclear, however, whether the magnitude of the observed decrease in plasma glutamine concentration would be great enough to compromise the function of immune cells. In fact, intracellular glutamine concentration may not be compromised when plasma levels are decreased postexercise. In addition, a number of recent intervention studies with glutamine feeding demonstrate that, although the plasma concentration of glutamine is kept constant during and after acute, strenuous exercise, glutamine supplementation does not abolish the postexercise decrease in in vitro cellular immunity, including low lymphocyte number, impaired lymphocyte proliferation, impaired natural killer and lymphokine-activated killer cell activity, as well as low production rate and concentration of salivary IgA. It is concluded that, although the glutamine hypothesis may explain immunodepression related to other stressful conditions such as trauma and burn, plasma glutamine concentration is not likely to play a mechanistic role in exercise-induced immunodepression

ambroziak - nie wierzę by glukozamina możnabyło zastepować leki. Co do lobby - to oczywiscie można równiedobrze założyc - że glukosamina ma swoje. Zwłaszcza, że jak wspomniałem chondroityna - wypadała lepiej i poważne lobby famaceutyczne nie wypusciło swoich macek... tutaj w kwestii glukozaminy: Glukozamina wchłania się w 90%, ale nie ma jej śladu w plazmie krwi: Pharmacokinetics of glucosamine in man The pharmacokinetics of glucosamine sulfate (CAS 29031-19-4) was investigated in 6 healthy male volunteers (2 per administration route) using 14C uniformly labelled glucosamine sulfate and administering it in single dose by intravenous (i.v.), intramuscular (i.m.) or oral route. The results show that after i.v. administration the radioactivity due to glucosamine appears in plasma and is rapidly eliminated, with an initial t1/2 of 0.28 h. 1-2 h after administration the radioactivity due to glucosamine disappears almost completely and is replaced by a radioactivity originating from plasma proteins, in which glucosamine or its metabolites are incorporated. This radioactivity reaches a peak after 8-10 h and then declines with a t1/2 of 70 h. About 28% of the administered radioactivity is recovered in the urine of the 120 h following the administration and less than 1% is recovered in the feces. After i.m. administration similar pharmacokinetic patterns are observed. After oral administration a proportion close to 90% of glucosamine sulfate is absorbed. Free glucosamine is not detectable in plasma. The radioactivity incorporated in the plasma proteins follows pharmacokinetic patterns which are similar to those after i.v. or i.m. administration, but its concentration in plasma is about 5 times smaller than that after parenteral administration. The AUC after oral administration is 26% of that after i.v., or i.m. administration. The smaller plasma levels of radioactivity after oral administration are probably due to a first pass effect in the liver which metabolizes a notable proportion of glucosamine into smaller molecules and ultimately to CO2, water and urea. The results confirm previous investigations in rats and dogs showing that also in man glucosamine sulfate is a prodrug for glucosamine that is well absorbed after oral administration and that, after i.v, i.m. or oral administration, diffuses into several tissues, including bones and articular cartilages. Setnikar I; Palumbo R; Canali S; Zanolo G. Pharmacokinetics of glucosamine in man. Arzneim Forsch (GERMANY) 43:1109-13; 1993. Glukozamina v.s. Placebo. wynik? - remis... Randomized, controlled trial of glucosamine for treating osteoarthritis of the knee. Rindone JP, Hiller D, Collacott E, Nordhaugen N, Arriola G. Veterans Affairs Medical Center, Prescott, AZ 86313, USA. joseph.rindone@med.va.gov OBJECTIVE: To determine the effectiveness of glucosamine in reducing pain from osteoarthritis of the knee. DESIGN: Randomized, double-blind parallel trial of glucosamine 500 mg three times daily or a placebo for 2 months. SETTING: Veterans Affairs Medical Center, Prescott, AZ. PARTI****NTS: Ninety-eight patients aged 34 to 81 being treated for osteoarthritis of the knee. MAIN OUTCOME MEASURES: Pain intensity both at rest and while walking as assessed by a visual analog scale at baseline and after 30 and 60 days of treatment. RESULTS: Forty-nine patients were randomly allocated to each group. There was no statistical difference between the two groups in scores on the visual analog scale at 30 days for resting (mean score placebo group 3.5 vs 3.3 glucosamine group, P = 0.66) or walking (5.1 vs 5.3 , P = 0.69); there was also no difference at 60 days for resting (3.4 vs 3.2 , P = 0.81) or walking (4.9 vs 4.9 , P = 0.90). There was also no statistical difference between groups in the mean change from baseline in scores on the visual analog scale (mean change for walking at 60 days placebo group -1.5 vs glucosamine group -1.4 , P = 0.77). Two parti****nts taking glucosamine and 4 taking placebo withdrew from the study due to adverse side effects (P = 0.67). CONCLUSION: Glucosamine was no better than placebo in reducing pain from osteoarthritis of the knee in this group of patients. PMID: 10693368 Badanie trzecie: długotrwałe i specjalistyczne studium (212 osob) pomiaru szczeliny w chorym stawie kolanowym.Wynik? Po trzech latach suplementacji bądź glukozaminą, bądź placebo zanotowano minimalne różnice pomiędzy obiema grupami. Glukozamina więc, w przypadku bardzo długiego podawania może wykazywać pewną skutecznosć. Long-term effects of glucosamine sulphate on osteoarthritis progression: a randomised, placebo-controlled clinical trial. Reginster JY, Deroisy R, Rovati LC, Lee RL, Lejeune E, Bruyere O, Giacovelli G, Henrotin Y, Dacre JE, Gossett C. Bone and Cartilage Metabolism Research Unit (WHO Collaborating Center for Public Aspects of Osteoarticular Disorders), University of Liege, Belgium. jyreginster@ulg.ac.be BACKGROUND: Treatment of osteoarthritis is usually limited to short-term symptom control. We assessed the effects of the specific drug glucosamine sulphate on the long-term progression of osteoarthritis joint structure changes and symptoms. METHODS: We did a randomised, double-blind placebo controlled trial, in which 212 patients with knee osteoarthritis were randomly assigned 1500 mg sulphate oral glucosamine or placebo once daily for 3 years. Weightbearing, anteroposterior radiographs of each knee in full extension were taken at enrolment and after 1 and 3 years. Mean joint-space width of the medial compartment of the tibiofemoral joint was assessed by digital image analysis, whereas minimum joint-space width--ie, at the narrowest point--was measured by visual inspection with a magnifying lens. Symptoms were scored by the Western Ontario and McMaster Universities (WOMAC) osteoarthritis index. FINDINGS: The 106 patients on placebo had a progressive joint-space narrowing, with a mean joint-space loss after 3 years of -0.31 mm (95% CI -0.48 to -0.13). There was no significant joint-space loss in the 106 patients on glucosamine sulphate: -0.06 mm (-0.22 to 0.09). Similar results were reported with minimum joint-space narrowing. As assessed by WOMAC scores, symptoms worsened slightly in patients on placebo compared with the improvement observed after treatment with glucosamine sulphate. There were no differences in safety or reasons for early withdrawal between the treatment and placebo groups. INTERPRETATION: The long-term combined structure-modifying and symptom-modifying effects of gluosamine sulphate suggest that it could be a disease modifying agent in osteoarthritis. PMID: 11214126 I kolejne.Pojedynek glukozaminy i placebo. Znowu remis. A randomized, double-blind, placebo-controlled trial of glucosamine sulphate as an analgesic in osteoarthritis of the knee R. Hughes and A. Carr1 St Peter's Hospital, Chertsey, Surrey and 1 University of Nottingham, Nottingham, UK Objectives. A randomized, placebo-controlled, double-blind trial of the relative effectiveness of glucosamine sulphate and placebo in managing pain in osteoarthritis (OA) of the knee. Methods. Eighty patients with OA of the knee were recruited from a rheumatology out-patient clinic and received either glucosamine sulphate 1500 mg daily for 6 months or dummy placebo. The primary outcome measure was patients' global assessment of pain in the affected knee. Results. Area under the curve analysis for the primary outcome measure showed no difference between placebo and glucosamine . The placebo response was 33%. There was a statistically significant difference between groups in knee flexion (mean difference 13°, 95% CI -23.13 to -1.97), but this difference was small and could have been due to measurement error. Conclusions. As a symptom modifier in OA patients with a wide range of pain severities, glucosamine sulphate was no more effective than placebo.

Glutamina wykazuje aktywność immunostymulującą - to fakt. Jednak stosowane tutaj dawki, jak dobrze pamiętam, są raczej dosyć wysokie - przynajmniej - kilkunastogramowe. Możesz spróbować np. mniejszych dawek - kilkugramowych - z dodatkiem innych immunostymulatorów, takich jak witamina C i flawonoidy.

Haute. Z doświadczenia wiem, że dawki rzędu kilkunastu gram (np.15) są zupełnie wystarczające, jeżeli dodasz do tego jeszcze z 1000 mg witaminy C, ze 300 mg trokserutyny i 100 mg witaminy E.

Co do kurkumy - z tego co mi sie przypomina, to jest jedną z tych przypraw/składników, która aktywuje bardzo silny (enzym?) zwalczający wolne rodniki, tysiące, a nawet miliony razy skuteczniej niż wit C i E, selen, cynk itp.

Okej, to o czym pisałem. *** http://www.ajcn.org/cgi/content/abstract/90/1/95 Enteral administration of alanyl-glutamine contributes more to the de novo synthesis of arginine than does intravenous infusion of the dipeptide in humans 1,2,3,4,5 Gerdien C Ligthart-Melis, Marcel CG van de Poll, Mechteld AR Vermeulen, Petra G Boelens, M Petrousjka van den Tol, Cors van Schaik, Jean-Pascal De Bandt, Nicolaas EP Deutz, Cornelis HC Dejong and Paul AM van Leeuwen 1 From the Department of Surgery, VU University Medical Center, Amsterdam, Netherlands (GCL-M, MARV, PGB, MPvdT, CvS, and PAMvL); the Department. of Surgery, University Hospital Maastricht & Nutrition and Toxicology Research Institute Maastricht, Maastricht, Netherlands (MCGvdP, NEPD, and CHCD); and Clinical Biochemistry, Université Paris Descartes, Paris, France (J-PDB). 2 GCL-M and MCGvdP contributed equally to this work and share first authorship. 3 Supported by a grant from the Netherlands Organization for Health Research and Development to PGB (920-03-185 AGIKO) and by a grant from Fresenius-Kabi, Bad Homburg, Germany. 4 Present address for NEPD: Center for Translational Research on Aging & Longevity, Donald W Reynolds Institute of Aging, University of Arkansas for Medical Sciences, Little Rock, AR. 5 Address correspondence to PAM van Leeuwen, Department of Surgery, VU University Medical Center, PO Box 7057, 1007 MB Amsterdam, Netherlands. E-mail: pam.vleeuwen@vumc.nl. Background: We previously confirmed in humans the existence of a pathway of glutamine into citrulline and arginine, which is preferentially stimulated by luminally provided glutamine. However, because glutamine is unstable, we tested this pathway with a stable dipeptide of glutamine. Objectives: The objectives were to explore whether alanyl-glutamine contributes to the synthesis of arginine in humans and whether this depends on the route of administration. Design: The study was conducted under postabsorptive conditions during surgery. Sixteen patients received alanyl-glutamine enterally or intravenously together with intravenously administered stable-isotope tracers of citrulline and arginine. Blood was collected from an artery, the portal vein, a hepatic vein, and the right renal vein. Arterial and venous enrichments and (tracer) net balances of alanyl-glutamine and glutamine, citrulline, and arginine across the portal-drained viscera, liver, and kidneys were determined. Parametric tests were used to test results (mean &#177; SEM). P < 0.05 was considered significant. Results: Twice as much exogenous glutamine was used for the synthesis of citrulline when alanyl-glutamine was provided enterally (5.9 &#177; 0.6%) than when provided intravenously (2.8 &#177; 0.3%) (P < 0.01). Consequently, twice as much exogenous glutamine was used for the synthesis of arginine when alanyl-glutamine was provided enterally (5 &#177; 0.7%) than when provided intravenously (2.4 &#177; 0.2%) (P < 0.01). However, results at the organ level did not explain the differences due to route of administration. Conclusions: Alanyl-glutamine contributes to the de novo synthesis of arginine, especially when provided enterally. A stable-isotope study using a therapeutic dose of alanyl-glutamine is needed to investigate the clinical implications of this finding. Ogólne streszczenie: Badanie przeprowadzone w Holandii na Uniwersytecie Maastricht dowiodło, że suplementy zawierające alanilo-glutaminę stymulują produkcje argininy w organiźmie. Glutamina bierze udział - według naukowców - w syntezie 64% argininy. Dożylne stosowanie alanilo-glutaminy podwaja poziom argininy, a stosowane doustnie tego suplementu również wywiera klinicznie istotny efekt Zmieniony przez - MolderDist w dniu 2010-03-10 23:59:59

Faftag, jeżeli chodzi o suple vs sterydy - to widzę, że zmierzamy do jednego celu, tylko trochę innymi drogami. Cieszę się z tego i nie odmawiam racji Twoim argumentom. Zazwyczaj kreuję dwa rodzaje informacji - marketingową i merytoryczną, aby każdy z niech skorzystał - i przeciętny paker, i fizjoterapeuta czy student AWF-u. Ale przyjmuję krytykę - oczywiście! Z tą glutaminą Kaizena to chodziło mi o to, że na obronie supli korzystają wszyscy ich producenci - nie tylko Oli. Substratami do syntezy BCAA są niektóre krótkołańcuchowe kwasy tłuszczowe i - właśnie - glutamina. Informacji tych szukaj raczej w podręcznikach biochemii. Jeżeli dobrze pamiętam, to wszystko to wyczytasz np. w Biochemii Harpera. Faktycznie, egzystuje takie pojęcie, jak - aminokwasy względnie niezbędne - w odniesieniu do argininy i histydyny, co nie zmienia faktu, że zalicza się je do aminokwasów egzogennych. Jeżeli dobrze pamiętam, to chyba wszystkie witaminy powstają w ludzkim organizmie, poza witaminą C. A sztandarowe przykłady - to synteza witaminy A z karotenoidów czy witaminy D z cholesterolu.

W zasadzie powyzszy tekst stanowi ciekawą pointę, która jednoczesnie obrazuje Twój sposob myslenia. Mnie natomiast interesuja badania zblizone w swoich realiach do realiów mojej i wiekszosci forumowiczów rzeczywistosci. Wierz mi, że mało kto ciwczy w warunkach podonych do do myszy walczącej o życie w akwarium. The effects of high-dose glutamine ingestion on weightlifting performance. Antonio J, Sanders MS, Kalman D, Woodgate D, Street C. Sports Science Laboratory, University of Delaware, Newark, Delaware 19716, USA. The purpose of this study was to determine if high-dose glutamine ingestion affected weightlifting performance. In a double-blind, placebo-controlled, crossover study, 6 resistance-trained men (mean +/- SE: age, 21.5 +/- 0.3 years; weight, 76.5 +/- 2.8 kg(-1)) performed weightlifting exercises after the ingestion of glutamine or glycine (0.3 g x kg(-1)) mixed with calorie-free fruit juice or placebo (calorie-free fruit juice only). Each subject underwent each of the 3 treatments in a randomized order. One hour after ingestion, subjects performed 4 total sets of exercise to momentary muscular failure (2 sets of leg presses at 200% of body weight, 2 sets of bench presses at 100% of body weight). There were no differences in the average number of maximal repetitions performed in the leg press or bench press exercises among the 3 groups. These data indicate that the short-term ingestion of glutamine does not enhance weightlifting performance in resistance-trained men. PMID: 11834123 The effects of 8 weeks of creatine monohydrate and glutamine supplementation on body composition and performance measures. Lehmkuhl M, Malone M, Justice B, Trone G, Pistilli E, Vinci D, Haff EE, Kilgore JL, Haff GG. Department of Nutrition and Food Science, Auburn University, Auburn, AL 36849, USA. Twenty-nine (17 men, 12 women) collegiate track and field athletes were randomly divided into a creatine monohydrate (CM, n = 10) group, creatine monohydrate and glutamine (CG, n = 10) group, or placebo (P, n = 9) group. The CM group received 0.3 g creatine.kg body mass per day for 1 week, followed by 0.03 g creatine.kg body mass per day for 7 weeks. The CG group received the same creatine dosage scheme as the CM group plus 4 g glutamine.day(-1). All 3 treatment groups participated in an identical periodized strength and conditioning program during preseason training. Body composition, vertical jump, and cycle performances were tested before (T1) and after (T2) the 8-week supplementation period. Body mass and lean body mass (LBM) increased at a greater rate for the CM and CG groups, compared with the P treatment. Additionally, the CM and CG groups exhibited significantly greater improvement in initial rate of power production, compared with the placebo treatment. These results suggest CM and CG significantly increase body mass, LBM, and initial rate of power production during multiple cycle ergometer bouts. PMID: 12930166 ______________________________________________ Zmieniony przez - faftaq w dniu 2010-03-29 23:15:06

brakuje dowodów naukowych, wskazujących jednoznacznie na to, że sterydy anaboliczne przyczyniają się do rozwoju zdolności wysiłkowych sportowców - nie zgadzam się. Choć nie zgłebiałem tematu dokładnie, to jednak widziałem badania które potwierdzały iż stosowanie sterydów anabolicznych (testosteron) wyraznie zwiększa syntezę białek mięsniowych, poprawia siłę miesni. Badań przeprowadzonych na sportowcach - jest po prostu bardzo mało, (choc są, jesli dobrze pamietam miedzy innymi dwuletnie badanie na grupie kulturystów z kilkuletnim stażem). W kontekscie samego testosteronu - zauważ, ze i tak samego testosteronu (krotkie estry), raczej nikt do budowy masy nie używa. Byly też z tego co pamietam badania z lat 70 z uzyciem tzw "metanabolu". Sytuacja z glutaminą jest odwrotna: są badania, w tym przeprowadzane na sportowcach - ale ich wyniki są dla glutaminy raczej dobijające. Ten obrazek testosteron-glutamina wydaje mi się trochę naiwny. ____________________________________ Wprawdzie genom ludzki zawiera pełen komplet genów kodujących wszystkie enzymy, katalizujące syntezę wszystkich aminokwasów, to 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. Aminokwasy takie produkują oczywiście organizmy niższe, ale to wchodzi już w zakres biochemii porównawczej czy medycznej. Endogenna synteza aminokwasów z krótkołańcuchowych kwasów tłuszczowych jest też typowym zagadnieniem z zakresu biochemii medycznej czy porównawczej, gdyż ma znaczenie głównie dla przeżuwaczy i chorych z hiperamonemią. - to ujęcie aktualnie uważam za dośc klarowne i ku nie mu intuicyjnie bym sie skłaniał Zmieniony przez - faftaq w dniu 2010-03-31 10:08:06 Co do kwestii spożycia bialka, to osobiscie również uważam, iż przecenia sie role znacznych jego ilości w diecie osob uprawiających dyscypliny siłowe, zwłaszcza jesli ich starania ukierunkowane sa na wzrost masy mięsniowej. Zawyzona podaż bialek pokarmowych (pow 2g/kg m.c.), moze byc moim zdaniem zasadne w programach redukcji wagi przy ograniczonym pozyciu weglowodanów. Z resztą wiele badań wskazuje taki zabieg za zasadny nawet dla osob które stronią od aktywnosci fizycznej. Przypominam iż nie mówię tutaj o sporcie wyczynowym z silnym wspomaganiem farmakologicznym. Warto zwrócic też uwagę iż większosc 'zwyczajnych' podręczników z zakresu żywienia wyraźnie podkreśla brak fizjologicznej zasadności spożywania znacznych ilości kalorii, a usilne zwiekszanie masy ciała ponad pewien wskaznik BMI - jest wręcz patologią... Zmieniony przez - faftaq w dniu 2010-03-31 12:12:36

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. ______________________________________________________________ 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-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 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. ______________________________________________________________ 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} __________________________________ Testosterone restores sex drive and boosts muscle mass, making it central to 2 of society&#8217;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 __________________________________________________________________ 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. _______________________________________________________________________________ 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. _______________________________________________________________ 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 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. melmoore@utmb.edu Short term administration of testosterone stimulates net protein synthesis in healthy men. We investigated whether oxandrolone , a synthetic analog of testosterone, would improve net muscle protein synthesis and transport of amino acids across the leg. Six healthy men 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. _______________________________________________________ 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 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 ____________________________________________________________ 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

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-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-KIC in proteins of cirrhotic liver was increased compared with controls (0.25 +/- 0.04% of alpha-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-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.

Dobre, dobre, ale dalej jest to tylko sugestia, a nie potwierdzone badaniami twierdzenie. Starczy przebadać maratończyków dając im glutaminę po biegu (połowie placebo) i popytać, czy ich zjadło przeziębienie. Witamin C w takiej sytuacji działa, właśnie w ten sposób ją sprawdzano. Poziom wewnątrzkomórkowy to nie wszystko. zwłaszcza że nie wiadomo, czy po 2 tygodniowym spadku poziomu w osoczu nie leci też właśnie ten wewnątrzkomórkowy - były tak długie badania? Wynik badań i wnioski z reguły zależą od tego, kto za badania zapłacił.