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Tux said:
If you want to argue with me, do so on here. You don't need to give me red just because you disagree with my opinion.
If Anavar really shut you down hard enough to require PCT, then why is it that it's given to children and women? Pretty much anything you do can "shut you down", from sleeping 4 hours a night to having 10 drinks in one night.
1. Anavar does not aromatize.
2. It does not affect the body's natural testosterone production, even in high doses. *
3. It is prescribed without PCT
* reason is that it does not have a negative feedback mechanism on the hypothalamohypophysial testicular axis, meaning that during the intake of Oxandrolone, unlike during the intake of most anabolic steroids, the testes signal the hypothalamus not to reduce or to stop the release of GnRH (gonadotropin releasing hormone) and LHRH Luteinizing hormone releasing hormone).
Pease find me information proving that Anavar shuts you down to a degree that requires PCT, and I will admit that I was wrong.
I think we all can agree that var is a lightweight, and as such, shouldn't be a big deal to run after PCT to keep strength in check. I was thinking about doing the same thing after my next cycle, but ultimately decided that time off equaling time on was too important to me. I don't see any real harm in trying it out though.
Tux
Well-known member
Azul, it's not MY opinion, it's the opinion of almost every experienced bber as well as the entire medical community. Straight from the PDR, anavar in a dosage as low as 2.5mg/day will suppress LH bro. It's given to women and children b/c it's very low on the androgenic spectrum so sides are MINIMAL... still possible though. Anavar does indeed affect testosterone production, not just in high doses, but in low doses too. Why don't you try running var at 50mg/day for 2 months and check your test levels afterwards. If they're still even in the normal RANGE I'll admit you have a point, but they'll not only be low, they'll be HRT low. I wasn't trying to insult you bro, but you deserved red for giving out possibly dangerous misinformation.
Tux
Well-known member
For you, Azul. Medical proof that 15mg/day of oxandrolone shuts young males down in only 5 days. You better apologize now 
Short-Term Oxandrolone Administration Stimulates Net Muscle Protein Synthesis in Young Men1
Melinda Sheffield-Moore, Randall J. Urban, Steven E. Wolf, J. Jiang, Don H. Catlin, David N. Herndon, Robert R. Wolfe and Arny A. Ferrando
Departments of Surgery (M.S.-M., S.E.W., D.N.H., R.R.W., A.A.F.), Anesthesiology (R.R.W.), and Internal Medicine (R.J.U., J.J.), University of Texas Medical Branch, and Shriners Burn Hospital for Children (D.N.H., R.R.W.), Galveston, Texas 77550; and the Department of Molecular and Medical Pharmacology, University of California, Olympic Analytical Laboratory (D.H.C.), Los Angeles, California 90025
Abstract
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.
Results
As depicted in Table 1, arterial steady state was achieved during the sampling hour (240–300 min) of both the control period and after 5 days of OX administration. However, arterial enrichments were significantly higher after OX treatment (Table 1; P < 0.05). Due to noncompliance with medications by one subject, all data presented include only the results from five subjects.
Serum OX concentrations on day 3 (1.9 ± 0.4 ng/dL) and day 5 (2.2 ± 0.3 ng/dL) of OX administration, measured 10 h after each evening’s oral dose (2100 h), remained steady. However, by 18 h posttreatment on day 5, serum OX levels were markedly reduced (0.48 ± 0.06 ng/dL; P < 0.01) compared to day 3 or day 5 10-h values. Total serum T concentrations were within normal physiological range on day 0 (449 ± 35 ng/dL) and day 3 (441 ± 44 ng/dL) of OX treatment. However, by day 5, total serum T concentrations were significantly reduced (282 ± 45 ng/dL; P < 0.05) below day 0 and day 3 values (Fig. 3). Serum free T concentrations were within normal physiological range on days 0, 3, and 5. However, by day 5, serum free T concentrations were significantly reduced (98 ± 10 pg/mL; P < 0.001) below day 0 (121 ± 12 pg/mL) and day 3 (126 ± 9 pg/mL) values. Hence, the total androgen concentration (T + OX) was reduced in parallel to the reduction in T (Fig. 3)....(continued)....
Discussion
We examined the response of muscle protein kinetics to OX administration in normal young men. We demonstrated that a moderate dose of OX, given over 5 days, stimulated muscle protein anabolism in young men. Further, we demonstrated for the first time in humans an increase in skeletal muscle ARs after anabolic intervention. Muscle anabolism during OX treatment occurred by stimulation of protein synthesis, as protein breakdown was unchanged. Moreover, a significant decrease in model-derived outward transport (FV,M) along with the calculated increase in protein synthetic efficiency indicate increased intracellular reutilization of amino acids. Taken together, these results demonstrate the mechanism of OX’s anabolic properties in fasted skeletal muscle.
A recent study from our laboratory (7) demonstrated that 5 days after a single im injection of TE (200 mg), FSR and model-derived protein synthesis increased 2-fold, with no change in FBR. Further, in agreement with the present findings, Ferrando et al. (7) demonstrated an increased utilization of intracellular amino acids by showing a strong relationship between protein breakdown and protein synthesis. Although our kinetic data strongly support these findings, the magnitude of the synthetic response with OX was not as great as that with TE. With OX, we found 44% and 28% increases in FSR and model-derived protein synthesis (FO,M), respectively. Several important factors may account for these differences.
In our previous study, the total T concentration increased to twice the physiological norm 2 days after TE injection (2094 ± 561 ng/dL). Further, T was still in the upper physiological range (953 ± 283 ng/dL) by day 5 and was statistically different from preinjection T concentration (425 ± 99 ng/dL) (7). In contrast, the magnitude of response we found in serum OX concentration was much less than that reported with TE. For example, total serum OX, as measured in the morning 10 h after oral ingestion, was consistent on days 3 and 5, whereas total serum and free T concentrations declined significantly from days 0 and 3 to day 5. Viewed in combination, total serum androgen levels with OX treatment were far below those obtained with TE. Although the total androgen exposure to the skeletal muscle with OX may have been considerably less than that we found previously with TE, an increase in protein synthesis was nonetheless observed. This suggests that OX may exert a greater anabolic influence on skeletal muscle than TE, thereby overcoming the decrease in the T concentration. ...(continued)...
Short-Term Oxandrolone Administration Stimulates Net Muscle Protein Synthesis in Young Men1
Melinda Sheffield-Moore, Randall J. Urban, Steven E. Wolf, J. Jiang, Don H. Catlin, David N. Herndon, Robert R. Wolfe and Arny A. Ferrando
Departments of Surgery (M.S.-M., S.E.W., D.N.H., R.R.W., A.A.F.), Anesthesiology (R.R.W.), and Internal Medicine (R.J.U., J.J.), University of Texas Medical Branch, and Shriners Burn Hospital for Children (D.N.H., R.R.W.), Galveston, Texas 77550; and the Department of Molecular and Medical Pharmacology, University of California, Olympic Analytical Laboratory (D.H.C.), Los Angeles, California 90025
Abstract
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.
Results
As depicted in Table 1, arterial steady state was achieved during the sampling hour (240–300 min) of both the control period and after 5 days of OX administration. However, arterial enrichments were significantly higher after OX treatment (Table 1; P < 0.05). Due to noncompliance with medications by one subject, all data presented include only the results from five subjects.
Serum OX concentrations on day 3 (1.9 ± 0.4 ng/dL) and day 5 (2.2 ± 0.3 ng/dL) of OX administration, measured 10 h after each evening’s oral dose (2100 h), remained steady. However, by 18 h posttreatment on day 5, serum OX levels were markedly reduced (0.48 ± 0.06 ng/dL; P < 0.01) compared to day 3 or day 5 10-h values. Total serum T concentrations were within normal physiological range on day 0 (449 ± 35 ng/dL) and day 3 (441 ± 44 ng/dL) of OX treatment. However, by day 5, total serum T concentrations were significantly reduced (282 ± 45 ng/dL; P < 0.05) below day 0 and day 3 values (Fig. 3). Serum free T concentrations were within normal physiological range on days 0, 3, and 5. However, by day 5, serum free T concentrations were significantly reduced (98 ± 10 pg/mL; P < 0.001) below day 0 (121 ± 12 pg/mL) and day 3 (126 ± 9 pg/mL) values. Hence, the total androgen concentration (T + OX) was reduced in parallel to the reduction in T (Fig. 3)....(continued)....
Discussion
We examined the response of muscle protein kinetics to OX administration in normal young men. We demonstrated that a moderate dose of OX, given over 5 days, stimulated muscle protein anabolism in young men. Further, we demonstrated for the first time in humans an increase in skeletal muscle ARs after anabolic intervention. Muscle anabolism during OX treatment occurred by stimulation of protein synthesis, as protein breakdown was unchanged. Moreover, a significant decrease in model-derived outward transport (FV,M) along with the calculated increase in protein synthetic efficiency indicate increased intracellular reutilization of amino acids. Taken together, these results demonstrate the mechanism of OX’s anabolic properties in fasted skeletal muscle.
A recent study from our laboratory (7) demonstrated that 5 days after a single im injection of TE (200 mg), FSR and model-derived protein synthesis increased 2-fold, with no change in FBR. Further, in agreement with the present findings, Ferrando et al. (7) demonstrated an increased utilization of intracellular amino acids by showing a strong relationship between protein breakdown and protein synthesis. Although our kinetic data strongly support these findings, the magnitude of the synthetic response with OX was not as great as that with TE. With OX, we found 44% and 28% increases in FSR and model-derived protein synthesis (FO,M), respectively. Several important factors may account for these differences.
In our previous study, the total T concentration increased to twice the physiological norm 2 days after TE injection (2094 ± 561 ng/dL). Further, T was still in the upper physiological range (953 ± 283 ng/dL) by day 5 and was statistically different from preinjection T concentration (425 ± 99 ng/dL) (7). In contrast, the magnitude of response we found in serum OX concentration was much less than that reported with TE. For example, total serum OX, as measured in the morning 10 h after oral ingestion, was consistent on days 3 and 5, whereas total serum and free T concentrations declined significantly from days 0 and 3 to day 5. Viewed in combination, total serum androgen levels with OX treatment were far below those obtained with TE. Although the total androgen exposure to the skeletal muscle with OX may have been considerably less than that we found previously with TE, an increase in protein synthesis was nonetheless observed. This suggests that OX may exert a greater anabolic influence on skeletal muscle than TE, thereby overcoming the decrease in the T concentration. ...(continued)...
Tux said:For you, Azul. Medical proof that 15mg/day of oxandrolone shuts young males down in only 5 days. You better apologize now
Short-Term Oxandrolone Administration Stimulates Net Muscle Protein Synthesis in Young Men1
Melinda Sheffield-Moore, Randall J. Urban, Steven E. Wolf, J. Jiang, Don H. Catlin, David N. Herndon, Robert R. Wolfe and Arny A. Ferrando
Departments of Surgery (M.S.-M., S.E.W., D.N.H., R.R.W., A.A.F.), Anesthesiology (R.R.W.), and Internal Medicine (R.J.U., J.J.), University of Texas Medical Branch, and Shriners Burn Hospital for Children (D.N.H., R.R.W.), Galveston, Texas 77550; and the Department of Molecular and Medical Pharmacology, University of California, Olympic Analytical Laboratory (D.H.C.), Los Angeles, California 90025
Abstract
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.
Results
As depicted in Table 1, arterial steady state was achieved during the sampling hour (240–300 min) of both the control period and after 5 days of OX administration. However, arterial enrichments were significantly higher after OX treatment (Table 1; P < 0.05). Due to noncompliance with medications by one subject, all data presented include only the results from five subjects.
Serum OX concentrations on day 3 (1.9 ± 0.4 ng/dL) and day 5 (2.2 ± 0.3 ng/dL) of OX administration, measured 10 h after each evening’s oral dose (2100 h), remained steady. However, by 18 h posttreatment on day 5, serum OX levels were markedly reduced (0.48 ± 0.06 ng/dL; P < 0.01) compared to day 3 or day 5 10-h values. Total serum T concentrations were within normal physiological range on day 0 (449 ± 35 ng/dL) and day 3 (441 ± 44 ng/dL) of OX treatment. However, by day 5, total serum T concentrations were significantly reduced (282 ± 45 ng/dL; P < 0.05) below day 0 and day 3 values (Fig. 3). Serum free T concentrations were within normal physiological range on days 0, 3, and 5. However, by day 5, serum free T concentrations were significantly reduced (98 ± 10 pg/mL; P < 0.001) below day 0 (121 ± 12 pg/mL) and day 3 (126 ± 9 pg/mL) values. Hence, the total androgen concentration (T + OX) was reduced in parallel to the reduction in T (Fig. 3)....(continued)....
Discussion
We examined the response of muscle protein kinetics to OX administration in normal young men. We demonstrated that a moderate dose of OX, given over 5 days, stimulated muscle protein anabolism in young men. Further, we demonstrated for the first time in humans an increase in skeletal muscle ARs after anabolic intervention. Muscle anabolism during OX treatment occurred by stimulation of protein synthesis, as protein breakdown was unchanged. Moreover, a significant decrease in model-derived outward transport (FV,M) along with the calculated increase in protein synthetic efficiency indicate increased intracellular reutilization of amino acids. Taken together, these results demonstrate the mechanism of OX’s anabolic properties in fasted skeletal muscle.
A recent study from our laboratory (7) demonstrated that 5 days after a single im injection of TE (200 mg), FSR and model-derived protein synthesis increased 2-fold, with no change in FBR. Further, in agreement with the present findings, Ferrando et al. (7) demonstrated an increased utilization of intracellular amino acids by showing a strong relationship between protein breakdown and protein synthesis. Although our kinetic data strongly support these findings, the magnitude of the synthetic response with OX was not as great as that with TE. With OX, we found 44% and 28% increases in FSR and model-derived protein synthesis (FO,M), respectively. Several important factors may account for these differences.
In our previous study, the total T concentration increased to twice the physiological norm 2 days after TE injection (2094 ± 561 ng/dL). Further, T was still in the upper physiological range (953 ± 283 ng/dL) by day 5 and was statistically different from preinjection T concentration (425 ± 99 ng/dL) (7). In contrast, the magnitude of response we found in serum OX concentration was much less than that reported with TE. For example, total serum OX, as measured in the morning 10 h after oral ingestion, was consistent on days 3 and 5, whereas total serum and free T concentrations declined significantly from days 0 and 3 to day 5. Viewed in combination, total serum androgen levels with OX treatment were far below those obtained with TE. Although the total androgen exposure to the skeletal muscle with OX may have been considerably less than that we found previously with TE, an increase in protein synthesis was nonetheless observed. This suggests that OX may exert a greater anabolic influence on skeletal muscle than TE, thereby overcoming the decrease in the T concentration. ...(continued)...
According to the study, total serum T concentrations were reduced to below day 0 values. The problem with the study is that it never gives total serum T concentrations before the study, so we have no baseline values to compare them to.
Ok, I apologize
I checked several sites to make sure that Anavar has no effect upon testosterone levels, and not a single one mentioned anything. Then I looked into some studies, and found a few similar ones to yours. OBJECTIVE: To investigate the effect of low dose oxandrolone and testosterone on the pituitary-testicular and GH-IGF-I axes. DESIGN: Prospective double-blind placebo-controlled trial. PATIENTS: Sixteen boys with constitutional delay of growth and puberty (CDGP) with testicular volumes 4-6 ml were randomized to 3 months treatment: Group 1 (n = 5), daily placebo: Group 2 (n = 5), 2.5 mg oxandrolone daily or Group 3 (n = 6), 50 mg testosterone monthly intramuscular injections with assessment (growth, pubertal development and overnight hormone profiles) at 0, 3, 6 and 12 months. MAIN OUTCOME MEASURES: LH and GH profiles (15-minute samples) were analysed by peak detection (Pulsar), Fourier transformation and autocorrelation. Testosterone levels were measured hourly and insulin, SHBG, IGF-I, and IGFBP-3 levels at 0800 h. Statistical analysis was by multivariate analysis of variance for repeated measures. RESULTS: LH and testosterone parameters increased significantly with time in all 16 (LH AUC, P < 0.001; peak amplitude, P = 0.02; number of peaks, P = 0.02; testosterone AUC, P = 0.02; morning testosterone, P = 0.002). In Group 2, however, LH and testosterone parameters decreased at 3 months followed by a rebound increase at 6 and 12 months. SHBG levels were markedly reduced at 3 months (P = 0.006) and a wider range of dominant GH frequencies was present although GH AUC was not increased until 6 months, with an increase in GH pulse frequency but not amplitude. IGF-I levels were increased at both 3 and 12 months. In Group 3, pituitary-testicular suppression was not apparent, but GH levels increased with an increase in GH amplitude at 3 and 12 months. CONCLUSION: Oxandrolone transiently suppressed the pituitary-testicular axis and altered GH pulsatility. Testosterone increased GH via amplitude modulation.
You'll get your karma back as soon as I can give it to you.
Tux said:And for what it's worth, you'll get some green from me whenever I can. I know it's not much, but perhaps someday I'll have more power lol. You've earned my respect bro, not many guys admit they're wrong... hell I've had a terrible problem with it all my life! Friends?
Of course
van_wilder
New member
constructive post. this is why i'm here...no flaming...good work keep it up!
VW
VW
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