Category: anabolics


20 ml 0,2g/ml L-arginine HCL infusion by Fresenius-Kabi $15

Investigation of the effects of oral supplementation of arginine in the increase of muscular strength and mass

Gerseli Angeli
1, Turibio Leite de Barros1, Daniel Furquim Leite de Barros2 and Marcelo Lima3


Introduction: Oral administration of arginine has been associated with physical performance improvement due to probable decrease of muscular fatigue derived from the vasodilatation factor of the nitric oxide over the skeletal muscles.
Objective: to evaluate the effects of oral administration of L-Arginine during an exercise program with weights. Methods: 20 male individuals, randomly divided in two groups: A and B, were submitted to eight weeks of training with weights (three times per week). Group A used 3 grams of L-Arginine + vitamin C during the eight weeks and group B used only vitamin C (control group).
Results: After eight weeks of training, group A presented body weight values and lean mass significantly higher (p < 0.05), body fat percentage significantly lower (p< 0.05), and strength of lower limbs significantly higher (p < 0.05), while group B did not present significant differences for the same period.
Conclusion: Oral administration of arginine associated with a training program with weights increased the stimuli of the exercise to the skeletal muscles level, enabling hence, increase of
muscular strength and mass.


Insulin physiology

It is often stated that the primary benefit of insulin in bodybuilding is that it increases the uptake of glucose into muscle and further that this movement of glucose is insulin dependent. But that is not exactly true. It may not be widely known but it is clearly established that insulin is NOT needed for glucose uptake and utilisation in man and therefore glucose uptake is NOT insulin dependent

There is a sufficient population of glucose transporters in all cell membranes at all times to ensure enough glucose uptake to satisfy the cell’s respiration, even in the absence of insulin. Insulin can and does increase the number of these transporters in some cells but glucose uptake is never truly insulin dependent.

Stimulatory & Inhibiting actions

Through stimulating the translocation or movement of ‘Glut 4’ glucose transporters from the cytoplasm of muscle and adipose tissue to the cell membrane insulin increases the rate of glucose uptake to values greater than the uptake that takes place in the basal state without insulin.

When insulin is administered to people with diabetes who are fasting, blood glucose concentration falls. It is generally assumed that this is because insulin increases glucose uptake into tissues, particularly muscle. In fact this is NOT the case and is another error arising from extrapolating from in vitro rat data. It has been shown quite unequivocally that insulin at concentrations that are within the normal physiological range lowers blood glucose through inhibiting hepatic glucose production without stimulating peripheral glucose uptake. As hepatic glucose output is ‘switched off’ by the inhibiting action of insulin, glucose concentration falls and glucose uptake actually decreases. Contrary to most textbooks and previous teaching, glucose uptake is therefore actually increased in uncontrolled diabetes and decreased by insulin administration.

When insulin is given to patients with uncontrolled diabetes it switches off a number of metabolic processes (lipolysis, proteolysis, ketogenesis and gluconeogenesis) by a similar inhibiting action. The result is that free fatty acid (FFA) concentrations fall effectively to zero within minutes and ketogenesis inevitably stops through lack of substrate. It takes a while for the ketones to clear from the circulation, as the ‘body load’ is massive as they are water and fat soluble and distribute within body water and body fat. Since both ketones and FFA compete with glucose as energy substrate at the point of entry of substrates into the Krebs cycle, glucose metabolism increases inevitably as FFA and ketone levels fall (despite the concomitant fall in plasma glucose concentration).

Thus insulin increases glucose metabolism more through reducing FFA and ketone levels than it does through recruiting more glucose transporters into the muscle cell membrane.

NOTE: The above was taken from:

Mechanism of action of insulin in diabetic patients: a dose-related effect on glucose production and utilisation, Brown P, Tompkins C, Juul S & Sonksen PH, British Medical Journal 1978 1239–1242.

Anabolic effect

Through facilitating glucose entry into cells in amounts greater than needed for cellular respiration insulin will stimulate glycogen formation.

It is possible to increase muscle bulk and performance not only through increasing muscle glycogen stores on a “chronic” basis but also to increase muscle bulk through inhibition of muscle protein breakdown. Just as insulin has an inhibiting action in inhibiting glucose breakdown in muscle glycogen, it also has an equally important inhibiting action in inhibiting protein breakdown.

The evidence now indicates that insulin does NOT stimulate protein synthesis directly (this process is under the control of growth hormone (GH) and insulin-like growth factor-I (IGF-I)). It has long been known that insulin-treated patients with diabetes have an increase in lean body mass when compared with matched controls. This results from insulin’s inhibition of protein breakdown in muscle tissue.

Growth Hormone Anabolic Actions

GH’s major action is to stimulate protein synthesis. It is at least as powerful as testosterone in this effect and, as they both operate through distinct pathways, their individual effects are additive or possibly even synergistic. In addition to stimulating protein synthesis, GH simultaneously mobilises fat by a direct lipolytic action. Together, these two effects are responsible for the ‘partitioning’ action of GH whereby it diverts nutritional calories to protein synthesis, possibly through using the energy derived from its lipolytic action. It most likely stimulates protein synthesis through mobilisation of amino acid transporters in a manner analogous to insulin and glucose transporters.

IGF-I also acts directly to stimulate protein synthesis but it has a weaker lipolytic action. GH, IGF-I and insulin thus act in concert to stimulate protein synthesis.

GH and IGF-I act in a promoting manner to stimulate protein synthesis while insulin acts in its characteristic inhibiting manner to inhibit protein breakdown. Thus they are synergistic in their powerful anabolic action.

Insulin is essential for the anabolic action of GH. GH administration in the absence of adequate insulin reserves (as during fasting or in Type 1 diabetes) is in fact catabolic and its lipolytic and ketogenic properties can induce diabetic ketoacidosis. Thus GH and insulin are closely linked in normal physiology and it is of great interest to see that athletes have discovered ways in which this normal physiological dependence can be exploited to enhance performance.


Turns out that stanozolol, the good old “Winny”, has unique collagen synthesis stimulating properties, that no other steroid has..

Stimulation of collagen synthesis by the anabolic steroid stanozolol

Researchers: Falanga V, Greenberg AS, Zhou L, Ochoa SM, Roberts AB, Falabella A, Yamaguchi Y; University of Miami School of Medicine, Department of Dermatology, Miami, Veterans Affairs Medical Center, Florida, USA.

Source: J Invest Dermatol 1998 Dec;111(6):1193-7

Summary: In this report, we measured the effect of the anabolic steroid stanozolol on cell replication and collagen synthesis in cultures of adult human dermal fibroblasts. Stanozolol (0.625-5 micrograms per ml) had no effect on fibroblast replication and cell viability but enhanced collagen synthesis in a dose-dependent manner. Stanozolol also increased (by 2-fold) the mRNA levels of alpha1 (I) and alpha1 (III) procollagen and, to a similar extent, upregulated transforming growth factor-beta1 (TGF-beta1) mRNA and peptide levels. There was no stimulation of collagen synthesis by testosterone. The stimulatory effects of stanozolol on collagen synthesis were blocked by a TGF-beta1 anti-sense oligonucleotide, by antibodies to TGF-beta, and in dermal fibroblast cultures derived from TGF-beta-1 knockout mice. We conclude that collagen synthesis is increased by the anabolic steroid stanozolol and that, for the most part, this effect is due to TGF-beta-1. These findings point to a novel mechanism of action of anabolic steroids.

Discussion: I must first acknowledge that the commonly held belief is that anabolic steroids predispose an athlete to tendon rupture. This conclusion is drawn from animal studies showing that some steroids produce a larger, stiffer tendon in rats and that these steroid-induced tendons “fail” before the tendons from the control animals. The term fail refers to the breaking point.

The interesting thing about the present study is that the steroid stanozolol (Winstrol) had a different effect than testosterone. If you are a regular reader of MESO-Rx you should be well aware that not all steroids act in the same manner. And that because of subtle differences in there molecular structure they are able to elicit different responses. For example, Deca seems to act primarily through the androgen receptor (AR) where as Dianabol has effects beyond those associated with the AR.

Because synthetic steroids have differ in their chemical properties it should not be surprising that testosterone did not have the same effect as Winstrol. Winstrol increased collagen synthesis as opposed to testosterone which did not in this study. Interpreting the results of this study are more difficult than simply describing them. Other researchers have suggested that steroids cause a rapid increase in protein synthesis within tendon fibroblasts which results in fibroids or fibrous nodules within the tendon (Michna,1988). These fibroids alter the mechanical properties of the tendon perhaps predisposing it to rupture. It is also noted that during short term use of steroids there is an alteration in the alignment of collagen fibers which may also lead to rupture. Interestingly these alterations in collagen metabolism are transient with markers of collagen turnover returning more or less to baseline after 3-4 weeks of steroid administration (Karpakka,1992). These same researchers noted that low dose anabolics effect primarily muscle collagenous tissue with tendon being effected only at higher doses (i.e. 5 times the therapeutic dose) which would more closely represent what is needed by bodybuilders to put on mass.

The question remains, dose this mean that Winstrol will actually help prevent tendon injury or will it lead to bigger yet stiffer tendons prone to injury? It is difficult to take animal research and extrapolate the results to humans. Stanozolol is used therapeutically in humans to treat a variety of connective tissue and vascular disorders and its clinical effects suggest that it can modulate connective tissue breakdown in people. Despite being labeled as “ineffective” by many bodybuilders it is very popular among athletes. As with most hormones, dosage plays a role in what effects are seen, be they positive or negative. Hopefully future studies will shed light on the therapeutic effects of different steroids on tendons in humans.


Michna H Appearance and ultrastructure of intranuclear crystalloids in tendon fibroblasts induced by an anabolic steroid hormone in the mouse. Acta Anat (Basel) 1988;133(3):247-50

Karpakka JA, Pesola MK, Takala TE. The effects of anabolic steroids on collagen synthesis in rat skeletal muscle and tendon. A preliminary report. Am J Sports Med 1992 May-Jun;20(3):262-6


30x 1 mg Finpecia finasteride DHT blocker $28

If you are using a DHT blocker such as finasteride, dutasteride or natural substances like green tea or saw palmetto, fortunately it doesn’t mean that you are blocking the anabolic properties of testosterone.

Inhibition of 5{alpha}-reductase blocks prostate effects of testosterone without blocking anabolic effects

Stephen E. Borst,1,2 Jun Hak Lee,1 and Christine F. Conover2

1Department of Applied Physiology & Kinesiology, University of Florida, Gainesville; and 2Geriatric Research, Education and Clinical Center, Malcom Randall Veterans Affairs Medical Center, Gainesville, Florida

Submitted 12 July 2004 ; accepted in final form 26 August 2004

We studied the effect of the 5{alpha}-reductase inhibitor MK-434 on responses to testosterone (T) in orchiectomized (ORX) male Brown Norway (BN) rats aged 13 mo. At 4 wk after ORX or sham surgery, a second surgery was performed to implant pellets delivering 1 mg T/day or placebo pellets. During the second 4 wk of the study, rats received injections of MK-434 (0.75 mg/day) or vehicle injections. Treatment with T elevated serum T to 75% above that for sham animals (P = 0.002) and did not affect serum dihydrotestosterone (DHT) or serum estradiol. T treatment also caused an elevation of prostate T and a marked elevation of prostate DHT. During the second half of the study, ORX rats lost an average of 18.86 ± 4.62 g body wt. T completely prevented weight loss, and the effect was not inhibited by MK-434 (P produced a nonsignificant trend toward a small (5%) decrease in the mass of the gastrocnemius muscle (P = 0.0819). This trend was also reversed by T, and the effect of T was not blocked by MK-434. T caused a significant 16% decrease in subcutaneous fat that was not blocked by MK-434 (P caused a 65% decrease in urine excretion of deoxypyridinoline, a marker of bone resorption, and again the effect was not blocked by MK-434 (P fivefold increase in prostate mass, and the effect was almost completely blocked by MK-434 (P that 5{alpha}-reductase inhibitors may block the undesirable effects of T on the prostate, without blocking the desirable anabolic effects of T on muscle, bone, and fat.