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TESTOSTERONE MORE IS BETTER

Bigbuttchicks

Member
I think this was posted a while back but this was one of the best articles I have read on testosterone use for performance enhancement! I guess more really is better. Another interesting finding in this is that IGF concentrations in the blood had NO correlation to leg press strength, it was strictly testosterone in the blood that concluded the findings. Enjoy!


Testosterone Dose-Dependently Increases Maximal Voluntary Strength and Leg Power, but Does Not Affect Fatigability or Specific Tension
Thomas W. Storer, Lynne Magliano, Linda Woodhouse, Martin L. Lee, Connie Dzekov, Jeanne Dzekov, Richard Casaburi and Shalender Bhasin
Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, California 90059

Address all correspondence and requests for reprints to: Thomas W. Storer, Ph.D., Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, 1731 East 120th Street, Los Angeles, California 90059. E-mail: [email protected].


Abstract
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References


Testosterone supplementation in men increases fat-free mass, but whether measures of muscle performance, such as maximal voluntary strength, power, fatigability, or specific tension, are improved has not been determined. Furthermore, the extent to which these measures of muscle performance are related to testosterone dose or circulating concentration is unknown. To examine the relationship between testosterone dose and muscle performance, 61 healthy, eugonadal young men (aged 18–35 yr) were randomized to 1 of 5 groups, each receiving a long-acting GnRH agonist to suppress endogenous testosterone production plus weekly injections of 25, 50, 125, 300, or 600 mg testosterone enanthate for 20 wk. These doses produced mean nadir testosterone concentrations of 253, 306, 542, 1345, and 2370 ng/dl, respectively. Maximal voluntary muscle strength and fatigability were determined by a seated leg press exercise. Leg power was measured using a validated leg power instrument. Specific tension was estimated by the ratio of one repetition maximum muscle strength to thigh muscle volume determined by magnetic resonance imaging. Testosterone administration was associated with a dose-dependent increase in leg press strength and leg power, but muscle fatigability did not change significantly during treatment. Changes in leg press strength were significantly correlated with total (r = 0.46; P = 0.0005) and free (r = 0.38; P = 0.006) testosterone as was leg power (total testosterone: r = 0.38; P = 0.007; free testosterone: r = 0.35; P = 0.015), but not muscle fatigability. Serum IGF-I concentrations were not significantly correlated with leg strength, power, or fatigability. Specific tension did not change significantly at any dose. We conclude that the effects of testosterone on muscle performance are specific; it increases maximal voluntary strength and leg power, but does not affect fatigability or specific tension. The changes in leg strength and power are dependent on testosterone dose and circulating testosterone concentrations and exhibit a log-linear relationship with serum total and free testosterone. Failure to observe a significant testosterone dose relationship with fatigability suggests that testosterone does not affect this component of muscle performance and that different components of muscle performance are regulated by different mechanisms.


Introduction
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References


THERE IS AGREEMENT that testosterone increases fat-free mass when given in physiological replacement doses to healthy, hypogonadal men (1, 2, 3, 4, 5, 6), to human immunodeficiency virus-infected men with low testosterone levels (7, 8, 9), and to older men with low normal testosterone levels (10, 11, 12, 13, 14). However, the data on the effects of testosterone replacement on measures of muscle performance are limited and somewhat contradictory. Some studies have reported greater improvements in grip strength in older men with testosterone supplementation than with placebo. In contrast, in a recent placebo-controlled, randomized clinical trial by Snyder et al. (12), testosterone treatment of older men did not increase muscle strength, even though testosterone administration was associated with gains in fat-free mass. In addition to muscle strength, both power (the rate of force generation) and fatigability (the ability of the muscle to persist in a task) are important measures of muscle performance. The effects of testosterone supplementation on muscle power and fatigability are unknown. Therefore, the first objective of this study was to comprehensively study the effects of testosterone administration on these important measures of muscle performance. We hypothesized that all three measures of muscle function, strength, power, and fatigability, would exhibit a linear response to testosterone dose.

An additional objective measure of qualitative muscle strength is specific tension, the force generated by each unit of muscle volume. Although strength is well accepted to be related to muscle size, it is not known whether testosterone administration induces changes in muscle strength in proportion to testosterone-induced hypertropic changes in muscle volume, or whether it has additional effects on the intrinsic contractile qualities of muscle that are independent of its effects on muscle mass. Therefore, we also determined the effects of testosterone administration on specific tension, a measure of the contractile quality of skeletal muscle, hypothesizing that muscle size and muscle strength would increase in parallel and in proportion to testosterone dose, thus resulting in no change in specific tension.

In a previous study we demonstrated that administration of supraphysiological doses of testosterone to healthy young men was associated with significant increases in muscle size and maximal voluntary strength (15). In contrast, Snyder et al. found no detectable changes in knee extension or knee flexion strength in either healthy, hypogonadal men or older men with low testosterone concentrations (12). Because the increments in testosterone concentrations were modest in the men treated with the testosterone patch used in this study (12), we considered the possibility that doses of testosterone higher than those used in studies of older men might be required to achieve improvements in muscle strength.

Recently, we used a Leydig cell clamp model to demonstrate for the first time that androgen-dependent processes differ in their testosterone dose-response characteristics (16). The details of the study design, the validation of this model, and the overall findings of this study have been published (16). The present manuscript describes the changes in three measures of muscle performance (voluntary muscle strength, power, and fatigability) as well as changes in muscle contractile quality (specific tension) as a function of testosterone dose.


Materials and Methods
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References


Study design

This was a double-blind, randomized study, approved by the institutional review boards of Charles Drew University and Harbor-UCLA Research and Education Institute. The details of the study design have been previously described (16). The study consisted of a 4-wk control period, 20 wk of treatment, and a 16-wk recovery phase. Treatment consisted of monthly injections of a long-acting GnRH agonist (Decapeptyl, DebioPharm, Geneva, Switzerland) to suppress endogenous testosterone production plus weekly injections of one of five testosterone dosing regimens.

Subjects

A total of 61 healthy men, aged 18–35 yr, participated in this study. All subjects had prior weight-lifting experience, but were not actively involved in strength training during the control or treatment phase of the study. Their characteristics at baseline are described in Table 1. Exclusion criteria included body weight greater than 20% above ideal weight for height, anabolic steroid use within the previous 12 months, or participation in competitive athletics within the previous 12 months. After signing informed consent, subjects underwent a physical examination, including digital rectal examination for evaluation of the prostate. Complete blood counts, blood chemistries, and prostate-specific antigen and serum testosterone levels were measured to determine eligibility. Those who met the eligibility criteria were randomly assigned to receive testosterone enanthate im each week in 1 of 5 testosterone dose regimens (25, 50, 125, 300, or 600 mg/wk). Randomization codes, using a block size of 5, were developed by our biostatistician and used for subject assignment to 1 of the 5 testosterone dose groups. Vials containing each of the 5 testosterone doses were prepared and coded by the research pharmacist. These coded vials were stored at the General Clinical Research Center (GCRC) and administered by GCRC nurses to assure compliance. Investigators, GCRC nurses, and subjects were blinded to the testosterone dose administered throughout the study period. All men received monthly injections of the long-acting GnRH agonist during the treatment phase, starting on d 1. The 5 testosterone doses were chosen such that, when administered weekly in combination with the GnRH agonist, they would produce nadir serum testosterone concentrations below, within, and above the physiological range. The doses selected were determined from published data and our previous experience with different testosterone doses.
 
Results
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References


Of the 61 subjects originally enrolled, 54 completed the study (16). One subject withdrew from the 25 mg/wk dose group, 4 from the 50 mg/wk dose group, and 2 from the 300 mg/wk dose group. None of these subjects withdrew because of adverse effects. Furthermore, none of the 54 subjects completing the study experienced serious adverse effects attributable to treatment.

The subjects’ baseline characteristics are presented in Table 1. Overall, our subjects averaged 26 yr of age with a body mass index (BMI) of 25 mg/wk. Although the subjects’ BMI was on the borderline between ideal weight for height and overweight as defined by current NIH recommendations (25), the subjects’ relative percentage body fat by underwater weighing (14%) indicated that, on the average, these men were lean. Their serum testosterone levels before treatment were in the midnormal range for healthy young men.

Hormone levels for these subjects have been previously reported (16). Mean ± SE serum total testosterone concentrations in the five groups, 7 d after previous testosterone injection (nadir levels), were 253 ± 66, 306 ± 58, 570 ± 75, 1345 ± 139, and 2370 ± 150 ng/dl, respectively; the corresponding free testosterone concentrations were 29 ± 5, 32 ± 3, 52 ± 8, 138 ± 21, and 275 ± 30 pg/dl, respectively. Serum total and free testosterone levels, measured during the last treatment week after the previous injection, were linearly related to the testosterone dose administered (P = 0.0001). In men receiving the 25- and 50-mg doses, nadir total and free testosterone concentrations decreased from baseline and were at the lower limit of the normal range for healthy young men. In contrast, serum total and free testosterone concentrations increased significantly from baseline and were in the supraphysiological range in men receiving the 300- and 600-mg doses. These values indicate that our experimental model was successful in creating graded ranges of serum testosterone concentrations. Mean ± SE changes in serum IGF-I were -7 ± 18, -17 ± 9, -18 ± 17, 58 ± 29, and 72 ± 13 ng/ml for the 25, 50, 125, 300, and 600 mg/wk testosterone doses, respectively (P < 0.001). Post hoc analysis indicted that the mean increase in the 600 mg/wk group was significantly greater than that in the 25, 50, and 125 mg/wk doses. The increase in the 300 mg/wk group was greater than that in subjects receiving the 125 mg/wk dose. The only statistically significant change from baseline was noted in subjects receiving the 600 mg/wk dose. The change in IGF-I was significantly related to testosterone dose (r = 0.50; P < 0.001).

Figure 1A illustrates individual changes in leg press strength within each of the five testosterone dose groups. Overall, changes in maximal voluntary strength in the leg press exercise were dependent upon testosterone dose and significantly correlated with both serum total (P = 0.0005) and free testosterone (P = 0.006) concentrations as illustrated in Fig. 1, B and C, respectively. Surprisingly, changes in leg press strength were not significantly correlated with circulating IGF-I concentrations (P = 0.22), as shown in Fig. 1D. The overall ANCOVA for change in leg press strength among the five treatment groups was significant (P = 0.0002). The changes in leg press strength from baseline in men treated with the 300 and 600 mg/wk testosterone doses were significantly greater than for the other three groups, but not significantly different from each other. Significant changes from baseline in leg press strength were observed in the 50, 300, and 600 mg/wk dose groups, but not for the 25 and 125 mg/wk groups.
 
displays individual subject changes in leg power with testosterone dose. Changes in leg power were dependent on testosterone dose and were significantly correlated with total and free testosterone concentrations during treatment (Fig. 2, B and C, respectively). However, as illustrated in Fig. 2D, changes in leg power were not significantly correlated with IGF-I concentrations. The overall ANCOVA for differences between dose groups was significant (P = 0.038). Post hoc analysis indicated that the mean change from baseline in the 600 mg/wk group was significantly greater than those in all the other groups (P < 0.05). The pattern of change in leg power was similar to that shown in Fig. 1A for strength, with the greatest increases in power noted for the 300- and 600-mg/wk dose groups (Fig. 2A). Both of these groups exhibited greater increases than subjects in the 25, 50, and 125 mg/wk groups.
 
Our data demonstrate that when the confounding factors in the measurements of muscle performance are controlled, testosterone administration increases maximal voluntary strength and leg power. In contrast, testosterone does not improve muscle fatigability, indicating that testosterone effects may be specific to certain characteristics of muscle performance, but not all. The effects of testosterone administration on muscle strength and leg power are dose and concentration dependent.

Previous studies of testosterone supplementation in androgen-deficient, young and older men have yielded conflicting results. Some studies in which physiological testosterone replacement was administered to healthy young hypogonadal men have reported significant gains in maximal voluntary strength and fat-free mass; however, a recent study reported no change in muscle strength after long-term testosterone administration even though fat-free mass increased significantly (4). The data on the effects of testosterone replacement in older men have also been contradictory. Tenover (13) and Sih et al. (26) reported that testosterone replacement of older men with low testosterone levels was associated with a greater improvement in grip strength than that associated with placebo administration. Recently, Ferrando et al. (11) reported significant gains in muscle strength in older men treated with testosterone. In contrast, in a well-designed, placebo-controlled, randomized clinical trial, Snyder et al. (12) found no significant differences in changes in knee extensor or knee flexor strength between placebo- and testosterone-treated men. The older men included in this study were not uniformly hypogonadal. In addition, their muscle strength was measured by a method (Biodex dynamometer) that did not demonstrate a response even in frankly hypogonadal younger men treated with testosterone (4). The Biodex dynamometer measures isokinetic strength using an open kinematic chain exercise that does not mimic natural movements in activities of daily living. Isokinetic strength, measured with an open kinematic chain exercise (leg extension) by this instrument, may assess a different measure of muscle performance than the variable resistance one-repetition maximum strength measured in the leg press exercise using the Keiser equipment with its closed kinematic chain movement. These data are consistent with the proposal that the effects of testosterone on muscle performance are specific to different measures of muscle performance. Therefore, failure of some previous studies to demonstrate improvements in some components of muscle performance should not be interpreted as evidence that testosterone has no effect on muscle performance. Our data provide unequivocal evidence that increasing testosterone concentrations in healthy young men are associated with dose- and concentration-dependent gains in maximal voluntary strength.

Our data constitute the first demonstration that testosterone improves leg power. Power is required in quick, explosive movements and has been shown to be correlated with functional activities in older persons (27, 28, 29, 30). Jozsi et al. (31) stressed the contribution of the decline in leg power to the age-related impairment of physical function. Kraemer and Newton (32) emphasized that the ability to generate power is the most important attribute of muscle performance in performing many sports and everyday activities. Because testosterone improves leg power, it is possible that testosterone might improve those aspects of physical function that are dependent upon leg power; this hypothesis needs to be tested in prospective studies.

Muscle fatigability was not significantly related to testosterone dose or serum concentration, although there was a trend toward significance. Although testosterone administration was associated with net accrual of muscle mass, additional peripheral adaptations, including increases in capillarization, mitochondrial density, and oxidative enzyme activity, that determine muscle fatigability might not be affected by testosterone. However, it is possible that the study did not have sufficient power to exclude a type II error (power for this test was 0.64).

The gains in maximal voluntary strength and muscle power were not significantly correlated with serum IGF-I concentrations. Observations that testosterone supplementation augments fat-free mass and muscle strength even in hypophysectomized men (1) suggest that testosterone-induced increases in circulating GH and IGF-I levels may not be essential for mediating testosterone effects on the muscle. It is possible that the increments in circulating GH and IGF-I concentrations during testosterone administration might indirectly contribute to nitrogen retention and augment the overall anabolic effects of androgens (33). Several studies are in agreement that testosterone directly stimulates im IGF-I mRNA and down-regulates respective binding proteins (34).

Our data show that testosterone administration alone increased maximal voluntary strength, but did not improve specific tension. Using similar methodology to determine specific tension, Welle et al. (23) reported significant 38% and 32% increases in knee extensor specific tension after 3 mo of resistance exercise training in their young (22–31 yr) and old (62–72 yr) subjects, respectively. Taken together, these data suggest that strength training improves the contractile quality of muscle, but testosterone does not. There are several important corollaries to these observations. First, the improvements in maximal voluntary strength during testosterone administration are proportional to the gains in muscle mass. Second, the mechanisms by which testosterone and resistance training each improves muscle strength must not be entirely similar. While there may be some common mechanistic pathways by which both testosterone and resistance exercise induce gains in muscle size and strength, the effects of resistance exercise on muscle function probably involve additional mechanisms that are not affected by testosterone.

We recognize that the errors in the measurement of both maximal voluntary strength and muscle volume contribute to variance in the estimates of specific tension. Although computerized tomography (35) and MRI (36, 37, 38) scans are often used to estimate muscle cross-sectional area or volume, these measurements will only be accurate in fibers that have a parallel orientation (10). Although we used an MRI-determined index of muscle size that has been found to correlate well with maximal voluntary isometric contractions (36), our in vivo estimates of specific tension may not reflect measurements obtained in vitro with individual muscle fibers. Because direct measurements of the length, diameter, and orientation of muscle fibers that are contributing to force generation cannot be made in vivo, some inherent, unmeasurable uncertainty in the estimates of specific tension in human studies is introduced (22). The present data, generated in healthy young men, are similar to those reported earlier in a frog model, in which castration or testosterone administration had no effect on specific tension (39).

This study demonstrates that gains in maximal voluntary muscle strength and muscle power are related to testosterone dose and to serum and free testosterone concentrations. A single log-linear, dose-response curve best described the relationship between circulating testosterone concentrations and changes in fat-free mass and muscle size. Our data are consistent with Forbes’s hypothesis of a linear relationship between testosterone dose and muscle mass and strength gains (4, 12, 13).

Generally, biological dose-response curves span a range of 2 log units. Within the constraints imposed by safety considerations, we only tested a relatively limited range of doses extending from 25–600 mg weekly. In light of what is known about biological dose-response curves, it is anticipated that a plateau would be achieved at doses that are approximately 2 log units higher than the minimal effective dose of testosterone enanthate. In that perspective, it is not surprising that a plateau was not observed within the relatively narrow range of doses that we studied. However, because of ethical and safety concerns, it is unlikely that doses higher than 600 mg would ever be tested in humans within the framework of a clinical research protocol.

The existence of a defined relationship between the administered dose and the gains in muscle strength and leg power suggests that in clinical disorders characterized by loss of muscle mass and function, it should be possible to predictably maximize gains in these measures of muscle performance by increments in testosterone dose. Our data predict that administration of supraphysiological doses to human immunodeficiency virus-infected men with weight loss, or men with cancer-associated cachexia would be associated with greater gains in muscle strength and power than those associated with physiological testosterone replacement. Although short-term administration of testosterone in physiological and slightly supraphysiological doses is relatively safe, the long-term effects of testosterone administration on the risk of prostate cancer and atherosclerotic heart disease are unknown. Long-term studies are needed to determine the range of serum testosterone concentrations that can be safely achieved to realize maximal anabolic effects without adversely affecting the risk to benefit ratio.

Our data were generated in healthy young men; we do not know whether similar dose-response relationships are operative in older men, men with chronic illness, or women. It is possible that testosterone dose-response curves might be shifted to the right in illness and old age. Testosterone dose-response relationships in women remain unknown.

The mechanisms by which testosterone exerts its anabolic effects on muscle function are not well understood, but probably involve alterations in the expression of many muscle growth regulators, including IGF-I, IGF-binding protein-3, and myostatin. Testosterone has also been shown to alter neuromuscular transmission. We do not know whether these effects are mediated through androgen receptor-mediated mechanisms or through an antiglucocorticoid effect. The effects of testosterone on muscle bioenergetics, capillarization and local blood flow, and mitochondrial function are not known and are the subjects of ongoing investigation
 
no im talking about the effects of supraphysiological doses of testosterone in normal men

if you read the article everyone you will enjoy it TURST ME!
it is a pain in the ass being so long though my bad haha
 
Bigbuttchicks said:
no im talking about the effects of supraphysiological doses of testosterone in normal men

if you read the article everyone you will enjoy it TURST ME!
it is a pain in the ass being so long though my bad haha
Click to expand...

supraphysiological= greater than normal. Hypergonadism, is production greater than normal... sounds like the same to me.
 
dude u missed the point the point was is the ATHLETES were right over the years. There was a scientific study done on STEROIDS. What we as lifters have wanted for years and better yet, the realtionship between doses and how they affect performance. It was a great article maybe you shoudl of read it
 
u know society is a sad world
dude if you dont like the article fine I dont give a ****
the fact of the matter is that this was an interesting article that some may enjoy
but I realize you guys think it is impossible to help someone read something interesting for once
this board really has some angry people on it jeeze
 
if you would have posted the abstract and the link to the whole study it would have been better. Most people only care about the conclusion and dont feel like reading the whole thing
 
Bigbuttchicks said:
u know society is a sad world
dude if you dont like the article fine I dont give a ****
the fact of the matter is that this was an interesting article that some may enjoy
but I realize you guys think it is impossible to help someone read something interesting for once
this board really has some angry people on it jeeze
Click to expand...

look at the way you are talking. I think you are the angry one. It is just a known fact that steroids are performance enhancing... hence why they are called "performance enhancing drugs".
 
yes but the article shows that a dose responsive vurve in strength so in proves wrong all the guys out there saying"a gram of test is just as good as two there is a law of diminishing returns"
or at least somehwat true
 
it shows that there is a dose responsive curve which is important because all the gurus claiming a gram of test to be good as two grams of testosterone just got their asses handed to them by science
How many time have we heard that "there is a law of diminishing returns and ther is apoint where more gear is useless"
 
"The effects of testosterone supplementation on muscle power and fatigability are unknown. Therefore, the first objective of this study was to comprehensively study the effects of testosterone administration on these important measures of muscle performance. We hypothesized that all three measures of muscle function, strength, power, and fatigability, would exhibit a linear response to testosterone dose."
 
Ok guy, for one thing, this study did not even reach a gram of Test, but rather 600mgs. And depending on the person, a gram of test and 600mgs would probably yield the same exact, if not similar gains.
 
It shows there is a doses/response curve between testosterone administration between 25 and 600 mg/week. It doesn't directly address the diminishing returns of very large doses since most people are talking about significantly more than 600 mg/week when they are talking about diminishing returns. These dose/response curves can't necessarily be extrapolated out indefinitely.
 
Bigbuttchicks said:
"The effects of testosterone supplementation on muscle power and fatigability are unknown. Therefore, the first objective of this study was to comprehensively study the effects of testosterone administration on these important measures of muscle performance. We hypothesized that all three measures of muscle function, strength, power, and fatigability, would exhibit a linear response to testosterone dose."
Click to expand...

Your understanding of science is astounding. I see a maximum dose of 600 mg per week not 1 or 2 grams per week. You can not extrapolate to higher doses. If you were familiar with the principles of pharmacology you would know that a linear dose response relationship is very rare and instead it usually looks like the graph below where at some dose, a maximal effect is reached.

Damn SRS beat me to it.
 

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"Ok guy, for one thing, this study did not even reach a gram of Test, but rather 600mgs. And depending on the person, a gram of test and 600mgs would probably yield the same exact, if not similar gains."

PLEASE tell me your joking right. Tell that to a top pro or amateur and you will get laughed out the door. A gram is better than 600 mg. Two grams is better than one gram BUT your are right in that as the benfits increase slightly, the sides increase dramatically. You are right to a point, but if you were accurate then why would people even bother taking over 600mg in the first place?

the unchecked
 
I have VERY close personal friends who are advising me some who are very good amateur bodybuilders and they have told me that the cream of the crop in this sport are using high amounts of test in the 2000-3000mg range to pack on sheer size. Maybe one or two other compounds at most. So I tell your graph to go **** itself
 
are you serious? what does any of what you said have to do with strength increases being dose dependent and an infinite amount of gear being best for everyone. think a 160lb guy would get more results from 2g than from 600mg
 
Just because people are doing it does not mean that it is correct -- mutual paranoia is common among professional athletes in that they feel that they have to do what the next guy s doing or they may fall behind. You also have to consider that as dose is increased you start to have a greater liklihood of off-target effects. And you are correct, there may be a slight increase in effectivness, however, the increase in incidence and severity of side effects is rapid.
 
Bigbuttchicks said:
"Ok guy, for one thing, this study did not even reach a gram of Test, but rather 600mgs. And depending on the person, a gram of test and 600mgs would probably yield the same exact, if not similar gains."

PLEASE tell me your joking right. Tell that to a top pro or amateur and you will get laughed out the door. A gram is better than 600 mg. Two grams is better than one gram BUT your are right in that as the benfits increase slightly, the sides increase dramatically. You are right to a point, but if you were accurate then why would people even bother taking over 600mg in the first place?

the unchecked
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Joking, not really mate... I do believe there is a point to were say 1 gram of test and 2 would yield the same gains, but the 2 grams of test would yield twice the sides...
 
ok you guys have made good points BUT
do you really think the top guys who are on 3 grams of test a week would be the smae size as now if they stuck with the 1000mg per week thinking "there is a law of diminishing returns"
No I am speaking about top guys and a 160 pound dude dont need a gram of test to start lol
As far as strength, the best powerlifters/strongman on the planet all use more than a gram of test
 
Bigbuttchicks said:
ok you guys have made good points BUT
do you really think the top guys who are on 3 grams of test a week would be the smae size as now if they stuck with the 1000mg per week thinking "there is a law of diminishing returns"
No I am speaking about top guys and a 160 pound dude dont need a gram of test to start lol
As far as strength, the best powerlifters/strongman on the planet all use more than a gram of test
Click to expand...

A much bigger guy will definitely need a higher dose but 3 grams is ridiculous. Also, you have to consider how much other stuff they are taking to maintain that size.
 
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