Stack per sviluppare massa muscolare

**shorinryu** · 11-07-2005, 09:26 PM

ora mi sono un po' scocciato di essere diplomatico: Tutto quello che scrivo e' documentato da trilioni di letteratura scientifica tr al' altro ti ho dato un po' di links circa il peso corporeo e non hai risposto.

prima di tutto erano linee guida, secondo ho sottolineato e ingrandito la parola almeno, e poi come al solito referenze alla mano quali sono le castronerie?

e i consigli pericolosi?

Neuroendocrinology. 2004 Jan;79(1):26-33.

Arginine increases growth hormone gene expression in rat pituitary and GH3 cells.

Adriao M, Chrisman CJ, Bielavsky M, Olinto SC, Shiraishi EM, Nunes MT.

Department of Animal Morphology and Physiology, Rural Federal University of Pernambuco, Recife, PE, Brazil.

The effect of arginine (Arg) and Ornitargin (OT) [a compound containing the aminoacids Arg, citrulline (Cit) and ornithine (Orn)] administration upon growth hormone (GH) gene expression was studied both in vivo and in vitro (hemipituitaries and GH3 cells) by Northern blot analysis. For in vivo studies, adult male Wistar rats were anesthetized, subjected to i.v. infusion of 200 microl of 150 mM NaCl (control group), Arg (15 or 150 mg) or OT (15 mg of Arg, 1 mg of Cit and 4 mg of Orn) at a rate of 20 microl/min, and killed 50 min thereafter. For the in vitro studies, hemipituitaries or GH3 cells were incubated in 1 ml of appropriate medium containing Arg (15 or 150 mg) or OT (15 mg of Arg, 1 mg of Cit and 4 mg of Orn) for 60 min. The pituitaries of the in vivo and in vitro studies and GH3 cells were subsequently processed for RNA extraction. Total RNA was subjected to electrophoresis in agarose (1%)/formaldehyde gel, transferred to a nylon membrane and subjected to hybridization with a rat GH (32)P-cDNA, and (32)P-18S rRNA probe to correct for the variability in RNA loading. After autoradiography of the membrane, the abundance of GH mRNA and 18S rRNA bands was quantified by densitometry. The in vivo study demonstrated that Arg and OT infusion induced a 2.3-fold increase in GH mRNA expression, which could result from the Arg-mediated inhibition of somatostatin release. In addition, in vitro Arg, but not OT, induced GH gene expression in hemipituitaries and GH3 cells, indicating that the aminoacid can act per se at the pituitary somatotrope level. In conclusion, our data show for the first time that arginine stimulates GH gene expression in parallel to its recognized GH-releasing activity. Copyright 2004 S. Karger AG, Basel

PMID: 14755131 [PubMed - indexed for MEDLINE]
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ZMA

RESEARCH SUPPORTIVE OF ZMA SUPPLEMENTATION

Effects of a Novel Zinc-Magnesium Formulation on Hormones and Strength

L.R. BRILLA1 AND VICTOR CONTE2
1Exercise and Sports Science Laboratory, Western Washington University, Bellingham, WA 98225-9067 and
2BALCO Laboratories, 1520 Gilbreth Road, Burlingame, CA 94010, Tel: 800-777-7122

L.R. BRILLA AND VICTOR CONTE. Effects of a Novel Zinc-Magnesium Formulation on Hormones and Strength. JEPonline, 3(4): 26-36, 2000. Muscle attributes and selected blood hormones of football players were assessed in response to a nightly supplementation regimen during spring football, over an 8-week period, with pre-post measures. A double-blind randomized study was conducted with ZMA (30 mg zinc monomethionine aspartate, 450 mg magnesium aspartate, and 10.5 mg of vitamin B-6) and placebo (P), n=12 and n=15, respectively. Plasma zinc and magnesium levels were ZMA (0.80 to 1.04 g/ml; 19.43 to 20.63 mcg/ml ) and P (0.84 to 0.80 g/ml ; 19.68 to 18.04 g/ml), respectively (P<0.001). Free testosterone increased with ZMA (132.1 to 176.3 pg/mL), compared to P (141.0 to 126.6 pg/mL) (P<0.001); IGF-I increased in the ZMA group (424.2 to 439.3 ng/mL) and decreased in P (437.3 to 343.3 ng/mL) (P<0.001). Muscle strength via torque measurements and functional power were assessed with a Biodex dynamometer. Differences were noted between the groups (P<0.001): ZMA (189.9 to 211 Nm at 180º/s and 316.5 to 373.7 Nm at 300º/s) and P (204.2 to 209.1 Nm at 180º/s and 369.5 to 404.3 Nm at 300º/s). The results demonstrate the efficacy of a Zn-Mg preparation (ZMA) on muscle attributes and selected hormones in strength-trained, competitive athletes.

Key Words: vitamin B6, anabolic hormones, testosterone, IGF-I, muscle

1. The effect of zinc depletion on muscle function was tested in 8 male subjects. After receiving 12 mg Zn/day for 17 days, the subjects received 0.3 mg Zn/day for either 33 or 41 days. The subjects were then divided into two groups for zinc repletion. Group A subjects received overnight infusion of 66 mg of Zn on Day 1 and 10 and then were fed 12 mg Zn/day for another 16 days. Group B subjects were fed 12 mg Zn/day for 21 days. Peak force and total work capacity of the knee and shoulder extensor and flexor muscle groups were assessed using an isokinetic dynamometer at baseline, at two points during depletion, and at repletion. Plasma zinc levels decreased by an average of 67% during depletion and remained 9% below baseline after repletion. The peak force of the muscle groups was not found to be significantly affected by acute zinc depletion, however, shoulder peak force (strength) was found to be reduced by 9.2% in the extensor muscles. Total work capacity (muscle endurance) for the knee extensor muscles and shoulder extensor and flexor muscles declined significantly by 28.1%, 24.1% and 26.4%, respectively. This study demonstrates that muscle endurance, or total work capacity, declines rapidly with acute zinc depletion and the degree of the decline was correlated with the reduction in plasma zinc concentration.

Van Loan, MD, et al. The Effects of Zinc Depletion on Peak Force and Total Work of Knee and Shoulder Extensor and Flexor Muscles. Int J of Sport Nutr, June 1999, Vol. 9, No. 2, 125-135.

2. A study was conducted to determine the effects of magnesium supplementation on strength development during a double-blind, 7-week strength training program in 26 untrained subjects (14=placebo, 12= Mg), 18-30 years old. Pre and post peak quadriceps torque (leg press) measurements were made using an isokinetic dynamometer. The leg muscle strength of the magnesium supplemented group significantly increased by 26%, compared to only 10% for the placebo group.

Brilla, LR, et al. Effect of Magnesium Supplementation on Strength Training in Humans. J Am Coll Nutr, July 1992, Vol 11, No. 3, 326-329

3. Serum zinc levels were determined in 160 training athletes (103 males and 57 females). In 23.3% of male and 43% of female athletes, serum zinc was significantly below the "normal range".

Haralambie, G. Serum zinc in athletes in training. Int J Sports Med 2 (1981) 135-138.

**shorinryu** · 11-07-2005, 09:38 PM

4. Magnesium, zinc and copper status of 270 US Navy Sea, Air and Land (SEAL) trainees was determined from dietary intakes and biochemical profiles. The dietary intakes of 34% and 44% of the trainees were below the RDA for Mg and Zn, respectively. The blood plasma concentrations of Mg and Zn were significantly below the "normal range" for 23% and 24% of the trainees, respectively.

Sing A, et al. Magnesium, Zinc and Copper status of US Navy SEAL trainees. Am J Clin Nutr 1989;49:695-700.

5. Serum zinc levels were measured in 20 adolescent gymnasts (9 boys, 11 girls, age 12-15). They had 26% lower serum zinc levels (0.599 +/- 0.026 mg/l) when compared to 118 matched controls (0.810 +/- 0.014, p < 0.001). The gymnasts serum zinc levels were positively correlated with adductor strength (r=0.468, p < 0.05). The 11 of 20 gymnasts with serum zinc < 0.6 mg/L had lower insulin-like growth factor binding protein 3 levels than the others (2.326 +/- 0.064 vs 2.699 +/- 0.12, p < 0.01). This protein is supposed to reflect growth hormone activity. Thus, zinc is lowered in trained adolescent gymnasts and this reduction could play a role in abnormalities of growth or muscular performance.

Brun J, et al. Serum zinc in highly trained adolescent gymnasts. Bio Trac Elem Res, 1995, Vol. 47, 273-278.

6. Twenty-one professional football (soccer) players underwent a maximal exercise test on a cycloergometer, with progressively increasing workloads until VO2max. On the whole these subjects had low serum zinc because nine (43%) of them had a hypozincemia (0.54 +/- 0.01 mg/L) which suggested a zinc deficiency. The subjects with low serum zinc had a 26% lower power output (123 +/- 8.71 vs. 166.27 +/- 14.84 watts, p = 0.029) and exhibited a 35% higher increase in blood lactate (lactic acid) during exercise (7.51 +/- 0.81 vs. 5.57 +/- 0.33 mmol/L, p <0.04) resulting in a 24% lower 2 mmol lactate threshold (44.7 +/- 3.9% vs. 58.9 +/- 4.8% of maximal power output p < 0.04). In conclusion, this study suggests that zinc status may influence blood rheology (flow) during exercise by an effect related to lactate accumulation.

Khaled S, et al. Serum zinc and blood rheology in sportsmen (football players. Clin Hemo and Micro 17 (1997) 47-48.

7. Ten collegiate basketball players serum mineral levels were measured before official practice began and immediately following the competitive season. Diets were monitored and remained the same throughout the four month period. Mean serum values for Mg and Zn decreased pre-season to post- season by 16% and 41%, respectively.

Lefavi RG, et al. Reduced serum mineral levels in basketball players after season. Med and Sci in Sports and Exer. Vol. 27, No. 5, May 1995

8. Twelve professional volleyball players and 12 control subjects were studied to determine the effects of daily physical training on serum, sweat and urine zinc concentrations. The professional athletes trained every day in two sessions, one in the morning (work in the gym for 2 hours) and another in the afternoon (specific work on the sports field for 3 hours). Simultaneously, 12 male volunteer university students, who were moderately trained, participated as the control group. The study was conducted over a period of 10 weeks. Pre-post tests were made using a progressive bicycle ergometer (increasing 30 W every 3 minutes to reach a maximum tolerated power). Pre-post blood samples were obtained at rest and immediately following exercise. After ten weeks of training, the professional athletes showed a significant increase in 24 hour urinary zinc excretion (22% greater losses), in contrast to a slight decrease (2% less) in the controls. The athletes also showed a very significant increase in the zinc loses in sweat compared to the controls. The athletes sweat zinc concentrations increased by an astounding 300%, compared to only 30% increases in the control group. The athletes serum zinc levels decreased by 4%, compared to a 2% decrease in the control group. Finally, the post exercise cortisol levels of the athletes significantly increased by 93%, compared to only an 18% increase in the controls. The authors stated that the athletes "cortisol levels increased in response to the exercise work load stress, and this behavior seems to be related to muscular damage". The authors went on to say that "It seems that the changes in zinc metabolism found in the study may be damage, increased protein turnover and increased zinc excretion (via sweat and urine). Because strenuous exercise during a period of competition can induce a "catabolic state" and has been shown to increase skeletal muscle protein turnover, it is likely that urine zinc is derived from muscle tissue". The authors concluded by saying that "Zinc supplementation and/or stress control appear to be indicated in athletes. In our practical opinion, we think that alterations in zinc metabolism with increases in zinc excretion and stress levels lead to a situation of latent fatigue with a decrease of endurance".

Cordova A, et al. Effect of training on zinc metabolism: changes in serum and sweat concentrations in sportsmen. Ann Nutr Metab, 1998 42:5, 274-82.

9. Plasma zinc, iron, copper and selenium levels were measured in 66 Navy SEAL trainees before and after a 5 day period of sustained physical and psychological stress called "Hell Week". The trainees pre-post plasma zinc levels decreased by 33%.

Singh A, et al. Biochemical indices of selected trace minerals in men: effect of stress. Am J Clin Nutrition 1991; 53:126-31.

10. Nine healthy, male subjects (18-40 years) were supplemented daily with 365 mg of magnesium as aspartate for 14 days. Before and after the supplementation period each subject performed a rigorously identical one hour ergometer exercise. The magnesium supplementation significantly reduced the subjects plasma levels of the catabolic "stress" hormone cortisol by an average of 25% (P < 0.025), which remained decreased during the exercise. The magnesium also significantly lowered the subjects' heart rates throughout the exercise period by an average of 8% (P < 0.03). Golf SW, et al. Plasma aldosterone, cortisol and electrolyte concentrations in physical exercise after magnesium supplementation. Clin Chem Clen Biochem, 1984, Vol. 22, pp. 717-721.

11. Medical students were tested to determine the acute effect of zinc supplementation on cortisol levels. The test was started at 7:00 AM after a 12 hour fast. Serial blood samples were collected from an experimental zinc group and controls at 30 minute intervals for 240 minutes. A subgroup of 7 subjects (3 men, 4 women) ingested 25 mg of zinc immediately after the baseline collection and their cortisol levels were compared to 8 matched controls who received a placebo. The control group started out with an average cortisol level of 11 mcg/dL and fell to 9 mcg/dL at 240 minutes, which is an 18% reduction. The zinc supplemented group started out with an average cortisol level of 16 mcg/dL and significantly dropped to 6.5 mcg/dL, which is a 59% reduction. In summary, the zinc supplemented group had a 41% greater reduction in cortisol levels compared to controls. The fact that zinc inhibits basal cortisol secretion in humans may be related to a direct blockade of cortisol synthesis and secretion in the adrenal cortex.

Brandao-Neto J, et al. Zinc acutely and temporarily inhibits adrenal cortisol secretion in humans. Bio Trace Elem Res, 1990, Vol. 24, 83-89.

12. Nine runners urine zinc and chromium levels were measured on a run day and compared to the levels on a non run day. The runners daily losses of zinc in urine were 50% greater on a run day compared to a non run day.

Anderson, R. Strenuous running. Bio Trac Elem Res, Vol. 6 (1984) 327- 336.

13. A percentage of testosterone is converted to dihydrotestosterone (DHT) by the enzyme 5a-reductase. An invitro study was conducted to determine the inhibition of 5a-reductase activity by zinc sulphate and azelaic acid. When added at concentrations of 3 or 9 mmol/l, zinc was a potent inhibitor of 5a-reductase activity. At a high concentration of 15 mmol/l, zinc completely inhibited 5a-reductase. The addition of vitamin B-6 potentiated the effect of zinc and resulted in a two-fold increase in the inhibition of 5a-reductase. A moderate concentration of 1.5 mmol/l of zinc in combination with 0.025% of vitamin B-6 inhibited the 5a-reductase activity by 90%. The zinc and vitamin B-6 combination may be effective at limiting DHT production and could represent a potential therapeutic agent in the treatment of androgen related pathology.

Stamatiadis D, et al. Inhibition of 5a-reductase activity in human skin by zinc and azelaic acid. Brit J of Derm, 1988, Vol. 119, pp. 627-632.

14. Androgen metabolism and aromatization, androgen and estrogen receptor binding and circulating levels of reproductive hormones were studied in zinc deficient rats. The zinc deficient group had significantly lower serum concentrations of testosterone (2.8 +/- .07 nmol/L) compared to the controls (8.7 +/- .07 nmol/L). This represents a remarkable 68% reduction in circulating testosterone levels. Scatchard analysis of the receptor binding data showed a significantly higher number of estrogen receptors in the zinc deficient group (36.6 +/- 3.4 fmol/mg protein) than in controls (23.3 +/- 2.4 fmol/mg protein) and a significantly lower number of androgen binding sites in rats fed the zinc deficient diet (6.7 +/- o.7 fmol/mg protein) than in controls (11.3 +/- 1.2 fmol/mg protein). To summarize, zinc deficiency caused a 41% reduction in the number of androgen binding sites and a 57% increase in the number of estrogen receptors. These findings indicate that zinc deficiency significantly reduces circulating testosterone concentrations and modifies sex hormone receptor levels.

Om AS, et al. Dietary zinc deficiency alters 5 alpha-reduction and aromatization of testosterone and androgen and estrogen receptors. J Nutr, 1996, Apr, 126:4,842-8.

15. Androgen binding was studied in zinc deficient rats. The experimental group of animals were maintained on a zinc deficient diet for 3 months. Scatchard analysis of the data revealed that the number of androgen binding sites in the zinc deficient rats was 31 +/- 5.2 fmol/mg cytosol protein. This was significantly lower than that (84 +/- 11.5 fmol/mg protein) of the controls. This 63% decrease in the number of androgen receptor cites in the zinc deficient state indicates that this metal is extremely important in the androgen binding process in the target cells.

Chung KW, et al, Androgen receptors in ventral prostate glands of zinc deficient rats. Life Sci,1986, Jan 27, 38:4, 351-356.

16. Nine men participated in an 85 day zinc depletion/repletion study divided into 3 metabolic periods: 18 day baseline, a 44 day depletion, and a 23 day repletion. 12 mg of zinc per day was fed to the men during baseline and were held constant after adjustments during the baseline period. Plasma zinc declined from 77.1 +/- 0.03 mcg/dl at baseline to 28.1 +/- 0.07 mcg/dl at depletion; concentrations returned to 77.9 +/- 0.03 mcg/dl at repletion. Total body weight, fat, fat-free mass (FFM), and bone mineral did not change during depletion, but total body water increased 5.3% +/- 1.9%, or about 2 kg or 4.4 lbs (P <0.05) by the end of the depletion and returned to baseline values at the end of repletion. The percent water in FFM increased from 71% +/- 1 to 75% +/- (P <0.05) at the end of depletion and was associated with a small decrease in body protein. The data suggest that zinc depletion impairs water balance.

Sutherland B, et al, Effect of experimental zinc depletion on body composition and basal metabolism in men. The FASEB Journal, Mar. 10, 1995, Volume 9, Number 4.

e potrei continuare a vita....

ma che cacchio dite

**shorinryu** · 11-07-2005, 09:53 PM

Su arginina http://www.nutriline.org/arginine.htm

Su ZMA http://www.nutriline.org/zma.htm
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Sul flax seed oil

ABSTRACTS

The rapid rate of postmenopausal bone loss is mediated by the inflammatory cytokines interleukin-1, interleukin-6, and tumor necrosis factor alpha. Dietary supplementation with flaxseeds and flaxseed oil in animals and healthy humans significantly reduces cytokine production while concomitantly increasing calcium absorption, bone calcium, and bone density. Possibilities may exist for the therapeutic use of the omega-3 fatty acids, as supplements or in the diet, to blunt the increase of the inflammatory bone resorbing cytokines produced in the early postmenopausal years, in order to slow the rapid rate of postmenopausal bone loss. Evidence also points to the possible benefit of gamma-linolenic acid in preserving bone density. (Kettler D, Altern Med Rev, 6(1): 61, 2001)

Results of many studies indicate that consumption of n-3 fatty acids can benefit persons with cardiovascular disease and rheumatoid arthritis. However, encapsulated fish oil is unlikely to be suited to lifetime daily use and recommendations to increase fish intake have not been effective. Foods naturally rich in n-3 fatty acids, such as flaxseed meal can be used to achieve desired biochemical effects without the ingestion of supplements or a change in dietary habits. A wide range of n-3-enriched foods could be developed on the basis of the therapeutic and disease-preventive effects of n-3 fatty acids. (Mantzioris E, et al, Am J Clin Nutr, 72(1): 42, 2000)

Many anti-inflammatory pharmaceuticals inhibit the production of eicosanoids and cytokines and it is here that possibilities exist for n-3 dietary fatty acids. Flaxseed oil contains n-3 fatty acid alpha-linolenic acid which can be converted after ingestion to eicosapentaenoic acid (EPA), which can act as a competitive inhibitor of AA conversion to PGE(2) and LTB(4), and decreased synthesis of these is observed after inclusion of flaxseed oil in the diet. Regarding the pro-inflammatory cytokines, tumor necrosis factor alpha and interleukins 1 beta, studies of healthy volunteers and rheumatoid arthritis patients have shown 90% inhibition of cytokine production after dietary flaxseed oil. (James M, et al, Am J Clin Nutr, 71(1 Suppl): 343S, 2000 )

It is essential in the process of returning n-3 fatty acids into the food supply that the balance of n-6/n-3 fatty acids in the diet that existed during evolution is maintained. Clinical investigations confirm the importance of n-3 fatty acids for normal function during growth and development and in the modulation of chronic diseases. Pregnant and lactating women and infants should benefit since their diet is deficient in n-3 fatty acids, especially for the vegetarians among them. Since cardiovascular disease, hypertension, and autoimmune, allergic, and neurological disorders appear to respond to n-3 fatty acid supplementation, a diet balanced in n-3 and n-6 fatty acids consistent with the diet during human evolution should decrease or delay their manifestation. (Simopoulos A, Lipids, 34, Suppl, 1999)

Human beings evolved consuming a diet that contained about equal amounts of n-3 and n-6 essential fatty acids. Over the past 100-150 years there has been an enormous increase in the consumption of n-6 fatty acids due to the increased intake of vegetable oils. Today, in Western diets, the ratio of n-6 to n-3 fatty acids ranges from approximately 20-30:1 instead of the traditional range of 1-2:1. Studies indicate that a high intake of n-6 fatty acids shifts the physiologic state to one that is prothrombotic and pro-aggregatory, characterized by increases in blood viscosity, vasospasm, and vasoconstriction and decreases in bleeding time. n-3 Fatty acids, however, have antiinflammatory, antithrombotic, antiarrhythmic, hypolipidemic, and vasodilatory properties. These beneficial effects of n-3 fatty acids have been shown in the secondary prevention of coronary heart disease, hypertension, type 2 diabetes, and, in some patients with renal disease, rheumatoid arthritis, ulcerative colitis, Crohn disease, and chronic obstructive pulmonary disease. Most of the studies were carried out with fish oils [eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)]. However, alpha-linolenic acid, found in green leafy vegetables (and especially) flaxseed, desaturates and elongates in the human body to EPA and DHA and by itself may have beneficial effects in health and in the control of chronic diseases. (Simopoulos A, Am J Clin Nutr, 70(3 Suppl) 1999)

Flaxseed, with 51-55% alpha-linolenic acid in its oil and its richest source of plant lignans, reduces hypercholesterolemic atherosclerosis by 46-69% without lowering serum lipids. (Prasad K, Atherosclerosis, 136(2): 367, 1998)

Use of flaxseed oil as a vegetative source of PUFA omega-3 in diet of patients with ischemic heart disease, hyperlipidemia and high blood pressure resulted in positive dynamic of clinical manifestation, blood lipids and coagulograms of the patient. Pronounced influence on membrane lipids of erythrocytes was revealed: significantly increased a quota an linolenic, eicosapentaenic and docosahexaenic PUFA against a background of reducing a level of linoleic acid. (Rozanova I, et al, Vopr Pitan, (5): 15, 1997)

The compliance or elasticity of the arterial system, an important index of circulatory function, diminishes with increasing cardiovascular risk. Dietary n-3 fatty acids in flax oil confer a novel approach to improving arterial function. (Nestel P et al, Arterioscler Thromb Vasc Biol, 17(6): 1163, 1997)

Naturally occurring polyunsaturated fatty acids (PUFA) are derived from (C18) linoleic and (alpha) linolenic acids, which cannot be synthesized by animals, but have to be derived directly or indirectly from plants. However, these acids are metabolised by animals from plants to form the omega 6 and omega 3 families of C20 and C22 PUFA and their physiologically powerful eicosanoids. The omega 6 eicosanoids generally produce such adverse effects as inflammation, clotting and promotion of cancer cell growth, and have an unfavourable influence on the immune system. In contrast, the omega 3 eicosanoids are anti-inflammatory, anti-clotting, retard the growth of cancer cells, and produce favourable effects on the immune system. The protective effects of omega 3 metabolites on coronary heart disease and cancer are relevant to the question of longevity. Polyunsaturated margarine is high in omega 6 fatty acids, and meat and milk products, high in omega 3 fatty acids, are however also high in cholesterol. (Shoreland F, Proc, Nutr Soc New Zealand, 17, CAB International, 1995) Flax bears the benefits without the risks.

**shorinryu** · 11-07-2005, 09:58 PM

Introduction

Flaxseed oil is a rich source of essential fatty acids (EFAs), particularly the omega-3 fatty acid alpha linolenic acid (ALNA). ALNA and linoleic acid (LA, an omega-6) are considered to be the two primary EFAs [1]. Other food sources rich in ALNA are some vegetable oils such as canola oil and soybean oil, walnuts, dairy products, beans, broccoli, and leafy greens. However, these sources generally do not contribute much ALNA to the diet, especially since soybean oil is usually partially hydrogenated, which decreases ALNA and increases trans fatty acid content [2]. Supplementation with flaxseed oil is a good way to increase the ALNA content of the diet, and multiple studies indicate that flaxseed or flaxseed oil favorably alters the tissue omega-6

mega-3 ratio [3-5]. Flaxseeds also have additional components, such as lignan precursors, which may play a role in preventing breast and other cancers [6], but these are not found in appreciable amounts in commercial flaxseed oil products.

There are numerous reasons why increasing dietary omega-3 fatty acid content is important. First, body stores of LA are high and can last for quite some time compared to ALNA, and the oxidation rate of ALNA is also higher. Intake of LA usually far exceeds requirements, and this is not the case with ALNA [1]. An imbalance between intake of omega-6 and omega-3 fatty acids is very common, especially in Western European and American populations [7], and this imbalance has been implicated in cardiovascular disease, depression, cancer, diabetes, arthritis and other inflammatory conditions, and other disease states and conditions [7-9]. This article will place the focus on the role of dietary ALNA on body composition and cardiovascular disease and compare ALNA to the longer-chain n-3 PUFAs (LC-PUFAs), docosohexaenoic acid (DHA) and eicosapentaenoic acid (EPA).

Arachidonic acid and lipogenesis

Arachidonic acid (AA) is an omega-6 fatty acid derived from LA. Although the conversion rate is low, the high intake of LA in most diets still affects AA concentrations [8]. Arachidonic acid is converted into specific leukotrienes, prostaglandins and thromboxanes, excessive production of which have been implicated in arthritis, asthma, cardiovascular disease, and other inflammatory disorders. Conversely, ALNA is metabolized into LC-PUFAs which competitively inhibit the AA cascade [7]. A role of EFA content in the diet on body fat is relatively well established in animals, although human research is still lacking. Dietary fats rich in ALNA and other omega-3's have both been reported to prevent adipose tissue development in rodents. Conversely, high tissue AA content has been implicated in promoting adipogenesis [10].

Arachidonic acid is a precursor to prostaglandin I2 (prostacyclin) via the cyclooxygenase (COX) pathway. Prostacyclin upregulates expression of two CCAAT-enhancer binding proteins, C/EBP-beta and C/EBP-delta, which then upregulate peroxisome proliferator-activated receptor gamma (PPAR-gamma); the functional consequence is that prostacyclin promotes adipogenesis in both rat and human preadipocytes. Prostacyclin also binds to PPAR-delta, and this may also lead to upregulation of PPAR-gamma. The fact that the adipogenic effect of AA can be reduced by COX inhibitors (such as aspirin) lends support to an important role in prostacyclin signalling in the development of adipose tissue. Dietary ALNA can decrease synthesis of AA from LA, through mechanisms such as competitive inhibition of the delta6 desaturase enzyme, and this could explain the reduction in fat mass seen in mice fed ALNA [10]. In addition, the LC-PUFA metabolites of ALNA can further stimulate fatty acid oxidation [11-12].

Cardiovascular disease

In confirmation of results from animal studies, epidemiological studies strongly suggest that ALNA, like EPA and DHA, reduces the risk of and fatality rates from cardiovascular disease. Mechanisms include prevention of arrhythmias, blood pressure reduction, anti-inflammatory effects, inhibition of platelet aggregation, and possibly a reduction in serum lipids [2, 13]. Epidemiological studies of various types find an association between increased intake of ALNA and lower risk of coronary artery disease and ischemic heart disease, lower risk of myocardial infarction, lower rate of cardiovascular disease mortality, and lower all cause mortality [1-2, 13-14]. Both primary and secondary prevention trials have provided further evidence for many of these benefits [13].

Not all studies have shown a benefit, however. Although the evidence is strong for most of the mechanisms of action, results from studies on the effect of ALNA on lipid profiles have been inconsistent [13-15]. The results from some epidemiologic studies are equivocal. This may be due to flaws or inconsistencies in study design [16]. It may also be because the effect of ALNA is more pronounced in populations with low intake of LC-PUFAs from fish. Finally, diets high in ALNA also tend to be high in trans fats, which increase cardiovascular disease risk and could confound results [2].

ALNA vs. EPA/DHA

The majority of the biological effects of ALNA are generally attributed to conversion to EPA and then DHA via desaturation and elongation. These fatty acids generally have all of the same benefits of ALNA, and then some. In human and animal studies, ALNA successfully raises tissue levels of EPA, but the conversion rate is low (less than 10%) [17]. The remaining ALNA is either beta-oxidized for other purposes or partitioned into certain tissues, such as skin [17-18]. The conversion rate to DHA is very low, so both ALNA and EPA supplementation generally fail to significantly increase tissue DHA content. It is likely that this is because DHA synthesis is regulated largely independently of tissue EPA content [17].

There is some debate over whether ALNA has important activity independently of its conversion to EPA/DHA, as the biological roles of ALNA are not well known. Research suggests that ALNA has independent anti-arrhythmic effects, effects on cholesterol metabolism and blood lipids, and anti-inflammatory effects [2, 16, 19-20]. In some tissues, such as the brain, ALNA may mimic some of the effects of the longer chain omega-3's [21]. ALNA may also play an important role in skin function [22].

Conclusion

Flaxseed oil is a good source of EFAs and a good way to change the omega-6/omega-3 ratio in the diet. It is associated with numerous health benefits. However, it is still debatable whether or not it will provide a benefit independent from EPA and DHA, which can be obtained in the diet through fish oil supplementation. Future studies may help to further define the biological role of ALNA.

**ham2** · 11-07-2005, 10:02 PM

io non sono certo il tale del "cibo è tutto e niente integratori", però certe affermazioni lasciano perplessi.
1 chilo al mese di massa magra è difficile anche per chi si fa le pere.
Se poi il concetto di "un chilo al mese" è preso alla bersagliera, allora anche strutto, pancetta, patate e maionese sono un buon stack.

L'arginina è roba vecchia di 20 anni ( il carrozzone di Saronno ) e lo ZMA è una "invenzione" di Richard Conte (?) e del clan Balco, noto più come steroid procurer & smuggler che altro.
Come certi pagliacci ora ripropongono aminoacidi AKG che Colgan consigliava nel 1994.
Zinco e magnesio sono ottimi composti; lo ZMA è una trovata commerciale ( lo studio sui marines è una boiata imperiale ).

Le accozzaglie di pubmed dicono ben poco anche agli esperti, figurarsi chi esperto non è. Ognuno ci vede quello che vuole, vedi Creatina, Glutamina etc dove per certi è un toccasana, per altri perdita di tempo, e tutti hanno gigabyetes di pubmed clutter da buttarsi in faccia.
Tant'è che il carrozzone di Saronno aveva inventato l'APL proprio sullo spunto di uno studio romano che non aveva chiarito se l'innalzamento del GH equivalesse ad aumento della massa magra o cosa.

**shorinryu** · 11-07-2005, 10:14 PM

be guarda quello che tu dice accozzaglia di MEDLINE e' il piu' grande database di ricerca internazionale di medicina e io lo utilizzo per lavoro all' universita'. Se non esci nel medline dove sono lisate le piu' prestigoise riviste accademiche non sei nessuno.

per quanto riguarda l' arginina che vuol dire perche' e' vecchia non funziona?

La risposta al protocollo e' individuale, dipende dall' eta', dieta, valori fisiologici ma posso dirti che molte persone usando questo protocollo hanno avuto successo. Poi anche li vale il ragionamento genetica

Almeno con te si puo' parlare, ma poi viene da ridere nel sentire flaxseed oil e' pericoloso MaH!!!

La creatine ethyl ester e' superiore alla creatina e porta un incremento di massa muscolare

comunque un altro interessante articolo sull arginina:

What is it and where does it come from?

Arginine is a semi-essential amino acid. It is a building block of protein that performs a myriad of physiological functions. It is a known precursor of the gas nitric oxide [N02].

Arginine is an amino acid that the body cannot make naturally. Therefore it is important to consume foods that are rich in arginine.1

Arginine is found in high concentrations in nuts and seeds like peanuts and almonds. It can also be found in chocolate and raisins. Dietary fiber is important because it keeps the digestive system functioning properly. It enhances our body's ability to use other dietary nutrients. Fiber goes through our digestive tract almost completely undigested. Once it reaches the colon and/or the large intestine, fiber is then broken down.

What does it do and what scientific studies give evidence to support this?

Arginine is necessary for the execution of many physiological processes. These physiological processes include hormone secretion, an increase in growth hormone output, the removal of toxic waste products from the body, and immune system defenses.2

Because Arginine is a precursor of nitric oxide [which is responsible for vasodiolation 3] it is often used for treating conditions such as chest cramping [angina], high blood pressure, heart disease, and sexual dysfunction. Arginine is also used in the treatment of male and female infertility.

Recently, dietary supplements containing Arginine have become popular due to Arginine's nitric oxide producing ability, its ability to scavenge free radicals, as well as its ability to signal muscle cells, release growth hormone, remove bad cholesterol, and enhance fat metabolism. Arginine helps regulate salt levels in the body. 4

For this reason it should be of interest to competing bodybuilders, as retaining water under the skin can make one looks smooth, bloated and washed out. The nitrogen retaining abilities of Arginine are well-known within the bodybuilding and scientific communities. Arginine is also believed to be crucial for muscle growth due to its vasodilating abilities, as well as its ability to participate in protein synthesis. 5

Who needs it and what are some symptoms of deficiency?

Everyone. Populations in particular need of arginine are growing children, infants, athletes, the obese or overweight, and the elderly. In adult populations Arginine is considered to be a non-essential amino acid. For children, by contrast, Arginine is essential to the defense and development of the adolescent immune system.

Persons suffering from injury can benefit from supplemental arginine, as demand for arginine is increased during times of bodily injury and repair.6 Persons suffering from erectile dysfunction or sexual dysfunction may also benefit from use of Arginine due to its vasodilating properties. In cases of erectile dysfunction or poor circulation of the extremities, Arginine will act to increase the diameter of blood vessels, thereby allowing increased blood flow to reach constricted areas.

Arginine presents benefits to hard training athletes. Supplementing with Arginine may boost the immune system, thereby allowing the athlete to train harder and avoid the detrimental effects of minor illnesses associated with overtraining.

Athletes who are discontinuing the use of androgenic or anabolic steroids may benefit from supplemental arginine because steroids often lead to hypertension, and the accumulation of bad cholesterol. Arginine has been shown to help reverse these conditions.

Due to Arginines ability to increase growth hormone levels, its ability to encourage lipid oxidization, its ability to lower blood pressure, and its ability to decrease arterial plaque, supplemental arginine may prove beneficial for obese persons.

How much should be taken? Are there any side effects?

Individuals with existing heart or psychiatric conditions should consult with their physician prior to supplementing with Arginine. With any amino acid containing product, overdose is a possibility. Dosing with too much arginine can lead to diarrhea, weakness and nausea. Clear dosing guidelines have not yet been established, so it is best to do what is known as "tolerance mapping".

Take a small dosage for one week, note the benefits and the side effects, and increase the dosage until the benefits are maximized and the side effects minimized. Over time the two will converge and you will hit the optimal dose. This process is similar to "receptor mapping" for bodybuilders who use insulin and steroids.

Many protein powders on the market are fortified with amino acids, including arginine. With this in mind, pay particular attention to how much arginine you are ingesting from sources. If you do not feel comfortable following the above described procedure, it is always best to follow the directions as prescribed on the products label.

REFERENCES

1. Alternative Medical Review. 2002, Dec;7 (6):512-22.
2. Appleton, J. 2002. Arginine: Clinical potential of a semi-essential amino.
3. Nakaki T; Kato R. 1994. Beneficial circulatory effect of L-arginine. Japanese Journal of Pharmacology. Oct, 66:2, 167-71
4. http://1001herbs.com/l-arginine/
5. Reyes AA; Karl IE; Klahr S Role of arginine in health and in renal disease [editorial] American Journal of Physiology, 1994 Sep, 267:3 Pt 2, F331-46
6. Albina JE, Mills CD, Barbul A, Thirkill CE, Henry WL Jr, Mastrofrancesco B, Caldwell MD. Arginine metabolism in wounds. American Journal of Physiology 1988;254:E459-E467.

Peace!

**shorinryu** · 11-07-2005, 10:23 PM

What is it and where does it come from?

Creatine Ethyl Ester HCL (CEE) is creatine monohydrate with an ester attached. Esters are organic compounds that are formed by esterification - the reaction of carboxylic acid and alcohols.

What does it do and what scientific studies give evidence to support this?
Regular creatine monohydrate has been shown effective at increasing lean muscle mass1,2,3,4, muscle strength5,6 and athletic performance.7,8

However, regular creatine monohydrate is absorbed poorly by the body - and its effectiveness is dependant upon the cells ability to absorb it. The poor absorption rate of regular creatine monohydrate requires the creatine user to ingest large dosages of creatine to achieve desired effect.

Because creatine draws water to the cell, and because most ingested creatine monohydrate is not absorbed, unabsorbed creatine will sit outside of the target cell with the water, and this will result in the "creatine bloat."

Long-term clinical studies have proven that creatine monohydrate is safe for use by persons free of medical complication9, but why would you want to ingest more creatine monohydrate than you have to simply because your creatine is inefficient?

Creatine ethyl ester is creatine monohydrate with an ester attached. The attachment of an ester is significant, because esters are found in the fat tissue of animals. But, why is this important? What role does this have in the absorption of creatine?

All substances that you put into your body will affect its operation. There are three ways that substances can affect a cells operation. They are:

Ligand binding to protein receptor sites.
Secondary messenger / metabotropic systems
Passive permeation of the cell wall via lipids
When a substance enters the body and affects the bodies operation, it is known as a ligand. The soma and dendrites of the cell have protein receptor sites to which ligands can bind. The process of a ligand binding with a receptor site is akin to a lock and key: only keys of a certain shape work with certain locks. When they work and cause the cells stimulation they are called agonists. When they block the cell from functioning they are called antagonists.

When a ligand binds with the receptor site of a target cell, the cell, in the simplest of cases, changes its shape, opens up its ion channels and changes its function. In so-called "secondary messenger" or metabotropic cells, the ligand binds with the receptor site and an internal protein known as a g-protein is released. This released protein then binds to an internal site inside of the cell, and then the cell changes its behavior by opening its ion channels. Cells that operate in this way are known as metabotropic cells because their operation requires metabolic energy.

Passive permeation is a process that describes the diffusion of a substance across a cell membrane through the use of lipids as transport mechanisms. Because no "work" is being done by the cell in this model, this model is called passive permeation.

Creatine monohydrate utilizes lipids to permeate the cell wall and enter the cell. Because of this, the esterification of creatine, and the presence of esters in animal fat tissue, becomes significant.

Creatine monohydrate is semi-lipopholic. This means that it inefficiently uses fat as a transport mechanism. The esterification of substances will increase their lipopholic abilities, and thus esterified creatine will use fat more efficiently to permeate the cell wall and exert its effects upon cellular function than its unesterified creatine monohydrate counterpart.

This means, simply, that not only will dosage requirements be lower, but the absorption of esterified creatine will be increased and the infamous "creatine bloat" will be eliminated!

Who needs it and what are some symptoms of deficiency?
Creatine Ethyl Ester can benefit persons of all ages, as it displays the same benefits as regular creatine monohydrate. Many multiple sclerosis patients are classified as creatine non-responders, but with the improved absorption seen with CEE this may not be the case.

REFERENCES

1. Racette SB. Creatine supplementation and athletic performance. J Orthop Sports Phys Ther. 2003 Oct;33(10):615-21.

2. Kreider, R.B., 1999. Dietary supplements and the promotion of muscle growth with resistance exercise. Sports Medicine 27:97-110.

3. Becque, M.D., et al. 2000. Effects of oral creatine supplementation on muscular strength and body composition. Medicine and Science in Sports and Exercise 32: 654-658.

4. Ingwal JS, Weiner CD, Morales MF, Davis E, Stockdale FE: Specificity of creatine in the control of muscle protein synthesis. J Cell Biol 63:145-151, 1974.

5. Rawson ES, Volek JS. Effects of creatine supplementation and resistance training on muscle strength and weightlifting performance. J Strength Cond Res. 2003 Nov;17(4):822-31.

6. Kambis KW, Pizzedaz SK. Short-term creatine supplementation improves maximum quadriceps contraction in women. Int J Sport Nutr Exerc Metab. 2003 Mar;13(1):87-96.

7. Gill ND, Hall RD, Blazevich AJ. Creatine serum is not as effective as creatine powder for improving cycle sprint performance in competitive male team-sport athletes. J Strength Cond Res. 2004 May;18(2):272-5.

8. Rawson, E.S., et al. 1999. Effects of 30 days of creatine ingestion in older men. European Journal of Applied Physiology 80: 139-144.

9. Sosin D.M., Sniezek J.E., Thurman D.J.. Incidence of mild and moderate brain injury in the United States, 1991. Brain Inj 1996 Jan;10(1):47-54.

vado un po' fuori tema ma anche da voi fa cosi' caldo!! A londra si crepa :

**^Squall^** · 12-07-2005, 01:06 AM

Originariamente Scritto da shorinryu

vado un po' fuori tema ma anche da voi fa cosi' caldo!! A londra si crepa :

Forse x via delle esplosioni.

**ham2** · 12-07-2005, 07:48 AM

[QUOTE ]be guarda quello che tu dice accozzaglia di MEDLINE e' il piu' grande database di ricerca internazionale di medicina e io lo utilizzo per lavoro all' universita'.[/QUOTE]

io dico che su siti americani tipo steroidology, muscletalk etc c'erano sapientoni che si spalavano merd@ addosso sostenendo opinioni contrapposte su tutto; naturalmente con pubmed, medline etc per terabyte a supporto.

Almeno con te si puo' parlare, ma poi viene da ridere nel sentire flaxseed oil e' pericoloso MaH!!!

io non ho detto niente al riguardo.

bisogna poi prendere passaggi da riviste scientifiche con cautela, perchè il parallelo tra atleti giovani in buona salute ed ustionati gravi, arteriosclerotici, feriti gravi, affetti da herpes anale o con chissà quale rara patologia, è molto esile.