WIN A X FACTOR T SHIRT or EVEN A CYCLE!!!

[jjohn]

DRUM ROLL!!!

Allright here's the deal! As promised, I'm goving away some goodies to my fellas. Because X Factor is the king of all anabolics, I will give you a chance to score a T Shirt, or even a CYCLE! Yeah, that's right! What you need to do is quite simple, answer the question:

What is inflamation, and how important is it to us, bodybuilders?

Make some research, and post it right in here, 10 shirts and 1 cycle will be given away!!!!!

Now go do some work!

[matic-]

first post do i win?

edit: whens the deadline

edit2:
Inflammation (from Latin word inflammatio - to set on fire) is the complex biological response of vascular tissues to harmful stimuli, such as pathogens, irritants, or in this case damaged muscle cells from lifting heavy. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue.

In the absence of inflammation, wounds, infections, and most importantly muscles would never heal or regenerate stronger and progressive destruction of the tissue would compromise the survival of the organism.
Inflammation can be classified as either acute or chronic. Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes from the blood into the injured tissues. A cascade of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue.

Acute Inflammation is involved when we talk about muscle hypertrophy. Heavy lifting done by us bodybuilders results in injury to skeletal muscle. The immune system responds with a complex sequence of immune reactions leading to inflammation. The purpose of the inflammation response is to contain the damage, and repair the damage. Macro****es, which are involved in ****ocytosis (a process by which certain cells engulf and destroy microorganisms and cellular debris) of the damaged cells, move to the injury site and secrete cytokines, growth factors and other substances. Cytokines are responsible for cell-to-cell communication.

To show how important macro****es are to muscle hypertrophy a strain of mice was recently genetically engineered to test the hypothesis of macro****e invasion to the site of injury is important for muscle regeneration and growth. A strain of mice was bred to be deficient in a protein called MCP-1 (Monocyte chemotactic protein-1), a potent activator for macro****e invasion and inflammation. Researchers damaged muscle fibers of these mice and compared them to normal mice; the mice that had impaired muscle macro****e activity due to a MCP-1 deficiency had impaired muscle regeneration and growth.

On a related note, NSAIDS or non-steroidal anti-inflammatory drugs are just as the name implies! ANTI INFLAMMATORY….They reduce the inflammation that is ever necessary for muscle hypertrophy. Ibuprofen blocks the action of the enzyme cyclooxygenase (COX). This enzyme causes pain and soreness, but also contributes to muscle growth.

From an article by M. G. Blennerhassett, P. Vignjevic, D. L. Vermillion and S. M. Collins entitled Inflammation causes hyperplasia and hypertrophy in smooth muscle of rat small intestine: “We investigated the association of structural change in the smooth muscle layers with inflammation. By day 6, smooth muscle area in cross sections of jejunum increased in longitudinal and circular muscle layers. The noninflamed ileum showed a smaller trophic response, with no significant change in area…thus extensive hypertrophy of smooth muscle cells are associated with inflammation.” While this study was on smooth muscle, it can surely be applied to skeletal muscle in the same sense. Growth factors are highly specific proteins that are involved in muscle hypertrophy. Growth factors stimulate the division and differentiation of a particular type of cell. Important growth factors associated with muscle hypertrophy include insulin-like growth factor (IGF), fibroblast growth factor (FGF), and hepatocyte growth factor (HGF). These growth factors work in conjunction with each other to cause skeletal muscle hypertrophy.

In conclusion muscular hypertrophy is a multidimensional process, with numerous factors involved. It involves a complex interaction of satellite cells, the immune system, growth factors, and hormones with the individual muscle fibers of each muscle all coming as a results of the inflammation caused by heavy lifting. Our bodies are highly adaptable, and will definitely adapt to the same routine over and over again. That is why it is important to switch it up every once in a while, say between high volume, and heavy weight, or even high reps. Or just switch up your exercises say use T-bar Rows or Chin-ups as your primary exercise for back instead of BB Rows or Deads once in a while. This change will continually keep the inflammation process coming on strong and in full force leading us to maximum muscle hypertrophy.

References:
1. Blennerhassett, M. G. "Inflammation causes hyperplasia and hypertrophy in smooth muscle of rat small intestine." American Journal of Physiology. 15 Nov 2007 <http://ajpgi.physiology.org/>.
2. The Mystery of Skeletal Muscle Hypertrophy by Richard Joshua Hernandez, B.S. and Len Kravitz, Ph.D.
3. MM.com
4. "Inflammation." Wikipedia: The Free Encyclopedia. 15 Nov 2007 <http://wikipedia.org>.

[cal62887]

Nice... There is a good article over at MM on this.

[Bolt10]

Nice... There is a good article over at MM on this.

yea i read that article...its a pretty good one

[jjohn]

first post do i win?

edit: whens the deadline

2 weeks. Feel free to edit, and add to your posts. Gotta give the chance to everyone.

[leonidas300]

The smart Answer

Exercise-induced muscle damage stimulates an acute-phase inflammatory response, which includes infiltration into skeletal muscle by macro****es1. Macro****es (Greek: ?big eaters?) are cells within the tissues that originate from specific white blood cells. One important role of macro****e is the removal of damaged tissue by heavy resistance exercise. Repairing damaged muscle cells is an important function of macro****es in the early stages of muscle damage and inflammation. This inflammatory response coincides with muscle repair, regeneration, and growth, which involves the activation of satellite cells (satellite cell activation is essential for muscle hypertrophy). The number of macro****es per square millimeter of muscle tissue is increased after heavy eccentric exercise compared to concentric exercise (lifting the weight) which may play an important role as to why eccentric contractions produce greater muscle hypertrophy2. Macro****es are also able to promote muscle growth and repair. In vitro studies (test tubes studies) show macro****es can increase muscle cell growth factors3,4, which indicates a role for macro****e-derived factors in muscle growth.


What happens if you suppress your ?Healing Factor??
The healing process that occurs during rest is an important adaptation to building muscle. You may be sore as hell after a heavy leg workout but that means your shocking your muscles into new growth. The inflammatory process although painful for a bodybuilder is an essential part of the muscle growth process. For instance, mediators such as IGF-1 are stimulated by the release of inflammatory cells5. So what happens if you suppress macro****es after injury? Just like Wolverine in the movies, if you lose your ?healing factors? you?re screwed in terms of building muscle. Researchers injected mice with an antibody that reduced macro****e concentrations after a couple of days of muscle overloading (86% reduction in macro****e concentration) and found that muscle fiber repair and growth was significantly impaired after muscle overload6. Macro****e-depletion also reduced muscle regeneration and prevented growth of muscle fibers that normally occurs with muscle overload. These findings suggest that macro****e first invades injured muscle serves to remove cellular debris, after which the subsequent invasive population participates in repair, regeneration and growth.

A strain of mice was recently genetically engineered to test the hypothesis of macro****e invasion to the site of injury is important for muscle regeneration and growth. A strain of mice was bred to be deficient in a protein called MCP-1 (Monocyte chemotactic protein-1), a potent activator for macro****e invasion and inflammation. Researchers damaged muscle fibers of these mice and compared them to normal mice; the mice that had impaired muscle macro****e activity due to a MCP-1 deficiency had impaired muscle regeneration and growth. The researchers speculated that the impaired muscle regeneration was due to macro****es not being able to repair the damaged muscle. Remember, muscle growth takes place during the recovery phase, lifting weights only serves as the stimulus. The research suggests that unless the damaged muscle fiber becomes invaded by macro****es and other repair mediators, it becomes stagnant and muscle repair is halted and the muscle tissue stays damaged. Interestingly, macro****es can increase nitric oxide which expands blood vessels and open up the muscle tissue to blood flow which allows for more macro****es to repair damaged muscle tissue10.

[leonidas300]

The body's inflamatory response after trainig is how your muscles repair themselves, adapt and therefore grow to accomodate future stress. without the inflamation following training the muscles would not be stimulated to heal or increase in size.

[leonidas300]

Inflammation is when you get sore after lifting heavy ass weights becuase everybody wanna be a bodybuilder but ain't nobody want to lift no heavy ass weight. We when ytou get sore from training like an animal that soreness is your body letting you know that is healing, and adpating, so you can get freakin swole!!!

[Alex08]

saving a spot for myself until completed.

[punksurfer024]

punksurfer's easy to read terms on inflammation and its effects on the bodybuilder:

inflammation is the bodies response to trauma. When the body is or in case of bodybuilders, muscles, are injured the inflammatory system is activated causing many things to happen. The blood vessels dialate, allowing more blood to deliver nutrients to areas that need it most. Blood cells carrying oxygen and nutrients are diverted from other areas to the injured area to speed recovery. Swelling occurs due to the increased blood to allow the area to have a constant supply of said nutrients. As the inflammatory response is activated so is the re-building process of the damage done (from workout). All these nutrients repair the muscle tissue helping it to grow, faster and stronger. For bodybuilders this is absolutly necessary, without it we wouldnt grow. The ability to activate the inflammatory system is very key to growth and size, if we are able to increase the effects of this system we will also increase the speed at which the muscle recovers and becomes stronger. There are many studies showing the bodies response to NSAIDs slowing the recovery and growth rates, in vise versa increasing the inflammatory response will do the opposite.

[jjohn]

Great start guys I like it!

[Eightpak]

This is a study done on the smooth muscle of a rat. Its not skeletal, but nontheless shows that hypertophy and even hyperplasia takes place in response to inflammation.


Inflammation of the rat jejunum with Trichinella spiralis causes altered smooth muscle contractility by day 6 postinfection (PI). We investigated the association of structural change in the smooth muscle layers with inflammation. By day 6 PI, smooth muscle area in cross sections of jejunum increased (P less than 0.05) in longitudinal (LM) and circular (CM) muscle layers. Nuclei counting in cross sections showed that cell number increased two- to threefold in CM and LM, and this increase was not reversed on day 23 PI. Estimation of cell size showed significant hypertrophy by day 6 PI in both muscle layers. [3H]thymidine autoradiography showed that the labeling index (LI) of jejunal LM and CM increased sharply on day 4 PI and peaked on day 6 PI (10- to 15-fold increase). The noninflamed ileum showed a smaller trophic response, with no significant change in area or nuclei number, the LI was increased only on day 6 PI in the ileal CM and was unchanged in LM. Thus extensive hyperplasia and hypertrophy of smooth muscle cells are associated with intestinal inflammation.

M. G. Blennerhassett, P. Vignjevic, D. L. Vermillion and S. M. Collins
Intestinal Disease Research Unit, McMaster University Health Sciences Centre, Hamilton, Ontario, Canada.

[Eightpak]

Arachidonic Acid and Site-Specific Muscle Growth
by William Llewellyn


Although building muscle without exercise may seem like the ideal endpoint of all anabolic research, this is a feat that just hasn?t been realized yet. There are a number of effective drugs and supplements for augmenting muscle growth, but resistance training is in inseparable part to the success of them all. This fact may be a ?given?, but have you ever wondered why that is? Why potent anabolic hormones simply do not build large amounts of muscle by themselves? Although the complete picture is not yet fully understood to science, the answer lies somewhere in the way the muscles respond to exercise; or more specifically, the changes in local chemistry that prime them for the actions of anabolic hormones. It is all about tissue specificity, and the body indeed is adept at directing anabolism only toward those muscles that require it. In this article we will take an up-close look at this tissue-specific response phenomenon, as well as examine the nutrient arachidonic acid, which seems to sit at the very center of it.



Exercise and Receptors


A good way to start off this discussion is to first look at the two hormones universally identified as those most integral to the building of muscle tissue, testosterone (representing the androgen class) and IGF-1 (insulin-like growth factor 1; the anabolic end product of GH). Elevation of either hormone, again, really only works well at promoting growth when training is also involved. Given the basic interaction between hormones and receptors, Bamman et al. set out in 2000 to see if receptor modification may play a key role in their tissue specificity[i]. The group of researchers open up their study noting, ?? transient elevations in serum anabolic factors such as growth hormones (GH) and testosterone have been documented after a bout of conventional resistance exercise? However, because the hypertrophic response is specific to the loaded muscle(s), activation by systemic hormone would require load-mediated modulation of the hormone?s efficacy in the exercised muscle. Load-mediated modulation of receptor expression or binding affinity in the muscle might explain localization of the growth response??



Bamman and company proceeded with the first in-depth examination of how androgen and IGF-1 receptor expression is changed in local tissues following exercise. The investigation involved 10 healthy male (7) and female (3) subjects, who were subject to bouts of eccentric and concentric resistance exercise and examined periodically for 48 hours after. Measures were taken of blood hormone levels, as well as local hormone receptor concentrations. The paper goes on to demonstrate some very interesting results. First, testosterone levels actually tended to decline in this study post-exercise. This was attributed to general as well as diurnal variation, the latter of which refers to the way testosterone levels fluctuate throughout the course of the day. IGF-1 levels did increase 48 hours after training, but only slightly (from 349 ng/dl to 416 ng/dl), and only with concentric training. Receptor concentrations, however, were a much different story. Both eccentric and concentric exercise produced significant increases in androgen and IGF-1 receptor concentrations. IGF-1 binding protein 4 (IGFBP-4) was also suppressed, which additionally would increase free IGF-1 and its biological activity. The results demonstrate that sensitivity to both testosterone and IGF-1 is markedly increased in local muscles following training, and present one way in which the body can ?direct? their anabolic actions.





Figure 1. The effect of eccentric resistance exercise on androgen receptor, IGF-1 receptor, and IGF-1 binding protein concentrations.



AA ? Root Trigger of Hypertrophy


So we have one proposed mechanism contributing to the localization of the growth response: receptor modulation. But how exactly does this modulation come about, and are other things involved too? Perhaps we should go back to the root. We need to see what is going on in your muscles during exercise, and how physiological changes during this window will shape growth in the hours and days to follow. It all begins with the damage caused to muscle fibers during resistance exercise. The coinciding cell disruption causes the release of phospholipase A2, which is responsible for liberating fatty acids from cell membranes. The main target of phospholipase A2 here is the polyunsaturated fatty acid arachidonic acid (AA), which is the most biologically active fatty acid towards skeletal muscle growth. Via the conversion of AA to prostaglandins (PGE2 and PGF2alpha), AA release will regulate protein synthesis and breakdown rates in local tissues, shifting them in favor of growth[i] [ii] [iii]. It is the first trigger in a very long and complex anabolic cascade.



Muscle growth involves more than just protein synthesis, however. For true hypertrophy to occur, immature satellite (stem) cells called myoblasts must be able to differentiate and fuse with mature muscle fibers. The process involves several steps. First, myoblasts are formed through cell proliferation, and stay stored on the outside of the cell. These mononucleated myoblasts will differentiate and fuse, forming a multinucleated immature cell (with several nuclei). This is usually referred to as a nascent myotube, and is the biological target of most molecules that effect muscle cell fusion. Immature myotubes then fuse with mature muscle cells, increasing myonuclear number and cell size. The myotubes will then continue to increase in size through normal protein accretion (protein synthesis). Through this, the growth and strengthening of the muscle fiber is achieved. Studies with PGF2alpha have shown this prostaglandin to strongly support hypertrophy at the second level of fusion, affecting the already formed nascent myotube by increasing its number of nuclei[iv]. This is a sufficient mechanism to support hypertrophy, and we must remember it is but one, and isolated to one (albeit a primary) metabolite of arachidonic acid. There are yet still other things at play.


AA and the AR


Although the link between arachidonic acid and muscle growth is well established, if, and how much, the AA cascade is directly involved with another specific aspect of the anabolic response, androgen receptor proliferation and local testosterone sensitivity in the muscles, has not (yet) been. However, there is support for the suspicion that there is a link, beyond the mere coincidence that both AA release and AR density increase during productive workouts. It lies in the examination of androgen receptor concentrations in other tissues. The first is a study on the drug flufenamic acid, which blocks inflammation by preventing arachidonic acid from converting to prostaglandins[v]. This drug was shown to markedly suppressed AR density and transcription in prostate cancer cells, which points to a directly related mechanism. However, because of speculation concerning other modes of action, a definitive conclusion was not made. Not long after, another study of interest was published, however. This one looked at the effects of essential fatty acids on gene expression in mice liver[vi]. After a diet rich in AA, androgen receptor concentrations were shown to increase more than 2.5 fold over control values. Yet another investigation took place about a year later. It was a follow up to the first investigation on flufenamic acid, which used more specific drugs[vii]. Here, the cyclooxygenase inhibitors celecoxib and nimesulide also suppressed androgen receptor levels in prostate cancer cells. Again, none of these studies may have been in skeletal muscle, but they do illustrate a strong effect in other tissues that may (likely) carry over here.



AA, IGF-1, and PI3K


Arachidonic acid is also a known stimulator of phosphatidylinositol kinase (PI3K)[viii]. Those familiar with the field of growth hormone research may recognize a key study published back in 1996, which looked at PI3K, and how it related to the protein synthesizing effects of both insulin and IGF-1[ix]. During this investigation, incubation of epitrochlearis muscle explants from mice with IGF-1 significantly increased both inward glucose transport and protein synthesis rates. This was an expected result given the hormone used, of course. But when the PI3K inhibitor wortmannin was added in with the IGF-1, both of these increases were quickly and effectively blunted. The researchers put it very succinctly when commenting ?Our results clearly demonstrated that stimulation of PI3 kinase was indispensable for the stimulatory effect of both insulin and IGF-1 on muscle protein synthesis.?

[Eightpak]

Exactly how AA affects PI3K and the IGF-1 signaling cascade is not entirely known. This does appear to be one of the most complex actions of arachidonic acid, and may involve the interaction of a number of its end products. It may include not only the cyclooxygenase metabolites of AA (prostaglandins), but lipoxygenase metabolite(s) as well, and perhaps involves both modulation of IGF-1 receptor density and signaling ability, through direct and indirect means[x] [xi] [xii] [xiii] [xiv]. Definitive studies in skeletal muscle tissue have not been undertaken, so no exact conclusions can be drawn. What is clear, however, is that arachidonic acid does affect this system, and likewise, should be intensifying the growth producing signals of not only androgens, but Insulin-Like Growth Factor 1 as well (endogenous or exogenous in origin). An in-depth examination of the IGF-1/PI3 kinase system would entail an article all of its own. If this interests you, a very good introduction can be found in the article “Behind The Scenes: Hypertrophy” by Gene, which can be found at this link.



http://www.avantlabs.com/page.php?pa...f=1&noupdate=1


Response Modulation


OK, so we know that arachidonic acid sits at the center of the core anabolic/hypertrophic response. Now, here comes the bad news. Levels of this nutrient can vary depending on a number of factors, and one of them happens to be exercise itself. A key effect of regular training is to diminish the responsiveness of the arachidonic acid cascade! This effect occurs via the gradual utilization of membrane-bound arachidonic acid, and its replacement with other fatty acids. As the arachidonic acid content is diminished, the body simply has less to use as substrate, and becomes less able to produce prostaglandins and other active metabolites. When this happens we seem to find it more difficult to trigger growth. It is also one of the reasons we are so much more receptive to training when we are first introduced to lifting, or when we hit the weights after a long period of time off.



Both ends of this equation have been well documented, but independently of one another. To begin with, studies with 19 sedentary middle-aged men in Sweden in 1998 showed that moderate exercise for as little as 6 weeks would measurably lower muscle AA content (it was largely replaced with oleic acid in this study)[xv]. On the other end of this phenomenon, we find a paper that was published about a decade earlier, which followed a group of athletes for one full year[xvi]. This study looked at this response using PGE2 as a marker, and reported a gradual and steady suppression of the prostaglandin system with regular exercise. The longer the subjects were on a regular training schedule, the harder it was for them to generate the same strong prostaglandin response (and logically other products of AA metabolism). Thankfully, dietary intake of AA can be modified (increased) to reverse (even exploit) this phenomenon. As you may be aware, I have been a strong advocate of AA loading for muscle building phases or training (X-Factor™), which is intended to increase AA levels and offer a strong pro-anabolic effect. It is a practice I am happy to say has been very effective, however I will save further product promotions for another time.



Summing It Up



We’ve merely touched on what is an extremely complex system in this article, and perhaps in doing so have raised more questions that we have answered. There is simply not enough time, space, or information to piece together a comprehensive look at the entire arachidonic acid/anabolic response cascade in one sitting. However, we can walk away with somewhat of a fundamental understanding of what is going on. Some main points of interest are summarized below for your review. As mentioned, this is an extremely large system to investigate, which leaves open room for a number of follow up articles with a different focus each. I’ll try my best to make sure more information is presented here, at Avant. Stay Tuned!





Key Points



? Arachidonic acid release/metabolism is the core regulator for muscle growth.

? AA metabolism increases protein synthesis rates, and also stimulates muscle hypertrophy.

? AA metabolism is tied to androgen receptor proliferation and testosterone sensitivity in certain tissues. This is speculated to include muscle.

? AA increases IGF-1 signaling via PI3K, and perhaps other mechanisms as well (speculated to include receptor proliferation in muscle).

? AA levels in skeletal muscle are decreased with regular resistance training.

? AA can be taken as a supplement to increase its stores in muscle tissue, in order to maintain maximum workout productivity and increase muscle hypertrophy.




References

[1] Mechanical load increases muscle IGF-1 and androgen receptor mRNA concentrations in humans. Bamman MM, Shipp JR, Jiang J. gower BA, Hunter GR, Goodman A, McLafferty CL Jr, Urban RJ. AM J Physiol Endogrinol Metab. 2001 Mar; 280(3):E383-90.

[1] Stretch-induced prostaglandins and protein turnover in cultural skeletal muscle. Vandenburgh HH, Hatfaludy S, Sohar I, Shansky J. Am J Physiol. 1990 Aug;259(2 Pt 1): C232-40.

[1] Effect of ibuprofen and acetaminophen on postexercise muscle protein synthesis. Trappe TA, White F, Lambert CP, Cesar D, Hellerstein M, Evans WJ. Am J Physiol Endocrinol Metab. 2002 Mar;282(3):E551-6.

[1] Skeletal muscle PGF(2)(alpha) and PGE(2) in response to eccentric resistance exercise: influence of ibuprofen acetaminophen. Trappe TA, Fluckey JD, White F, Lambert CP, Evans WJ. J Clin Endocrinol Metab. 2001 Oct;86(10):5067-70.

[1] Prostaglandin F2(alpha)stimulates growth of skeletal muscle cells via an NFATC2-dependent pathway. Horsley V, Pavlath GK. J Cell Biol. 2003 Apr 14; 161(1):111-8.

[1] A nonsteroidal anti-inflammatory drug, flufenamic acid, inhibits the expression of the androgen receptor in LNCaP cells. Zhu W, Smith A, Young CY. Endocrinology. 1999 Nov;140(11):5451-4.

[1] Dietary effects of arachidonic-rich fungal oil and fish oil on murine hepatic and hippocampal gene expression. Berger A, Mutch DM, Bruce German J, Roberts MA. Lipids Health Dis. 2002 Oct 21;1(1):2.

[1] The cyclooxygenase 2-specific nonsteroidal anti-inflammatory drugs celecoxib and nimesulide inhibit androgen receptor activity via induction of c-Jun in prostate cancer cells. Pan Y, Zhang JS, Gazi MH, Young CY. Cancer Epidemiol Biomarkers Prev. 2003 Aug;12(8):769-74.

[1] Arachidonic acid activation of translation initiation signaling in vascular smooth muscle cells. Neeli I, Yellaturu CR, Rao GN. Biochem Biophys Res Commun. 2003 Oct 2;309(4):755-61.

[1] Phosphatidylinositol 3-kinase and p70 s6 kinase participate in the regulation of protein turnover in skeletal muscle by insulin and insulin-like growth factor I. Dardevet d, Sornet C, Vary T, Grizard J. Endocrinology. 1996 Oct;137(10):4087-94

[1] Insulin-like growth factor-I antagonizes the antiproliferative effects of cyclooxygenase-2 inhibitors on BxPC-3 pancreatic cancer cells. Levitt RJ, Pollak M. Cancer Res. 2002 Dec 15;62(24):7372-6

[1] COX-2 Regulates the insulin-like growth factor I-induced potentiation of Zn(2+)-toxicity in primary cortical culture. Im JY, Kim D, Lee KW, Kim JB, Lee JK, Kim DS, Lee Yi, Ha KS, Joe CO, Han PL. Mol Pharmacol. 2004 Sep;66(3):368-76.

[1] Cyclooxygenase-2 modulates the insulin-like growth factor axis in non-small-cell lung cancer. Pold M, Krysan K. Pold a, Dohadwala M, Heuze-Vourc’h N, Mao JT, Riedl KL, Sharma S, Dubinett SM. Cancer Res. 2004 Sep 15;64(18):6549-55.

[1] Insulin and insulin-like growth factor-I responsiveness and signaling mechanisms in C2C12 satellite cells: effect of differentiation and fusion. Palmer RM, Thompson MG, Knott RM, Campbell GP, Thom A, Morrison KS. Biochim Biophys Acta. 1997 Feb 4;1355(2):167-76

[1] Five-lipoxygenase inhibitors can mediate apoptosis in human breast cancer cell lines through complex eicosanoid interactions. Avis I, Hong SH, Martinez A, Moody T, Choi YH, Trepel J, Das R, Jett M, Mulshin JL. FASEB J. 2001 Sep;15(11):2007-9. Epub 2001 Jul 9.

[1] Andersson, A, Sjodin A, Olsson R, Vessby B. Effects of physical exercise on phospholipid fatty acid composition in skeletal muscle. Am J Physiol. 1998 Mar;274(3 Pt 1):E432-8.

[1] Effects of exercise on parameters of blood coagulation, platelet function and the prostaglandin system. Sinzinger H, Virgolini I. Sports Med, 1988 Oct;6(4):238-45. Review.

[jjohn]

Eightpak, I'd like to see a post you wrote, not Bill's article :P

[user98511001541]

Inflammation is when you get sore after lifting heavy ass weights becuase everybody wanna be a bodybuilder but ain't nobody want to lift no heavy ass weight. We when ytou get sore from training like an animal that soreness is your body letting you know that is healing, and adpating, so you can get freakin swole!!!

x2

what do i win

[BiggerWeighter]

Those of you who read our web site regularly know that when it comes to the science of building muscle and shedding body fat, AST has always been one-step ahead in the industry. If you take a quick browse through the pages within this site, you see that we?ve been warning consumers about various scams often before they happen. We've also been recommending cutting-edge supplementation and training techniques often before they?ve been confirmed by research and long before other supplement companies have a clue.

Aside from introducing the most efficient bodybuilding training program in the world, Max-OT, AST introduced strength athletes to foundation products such ultra-high quality whey proteins, Creatine HSC and the most awesome caffeine/ephedra products (yes, AST has been around for that long!) AST was also advocating many bodybuilding strategies years before they became in-vogue, such as, high-intensity cardio exercise, supplement-timing and the strategic use of carbohydrates and various proteins at various times of the day.

AST is much more than a supplement company. Aside from producing the finest quality supplements in the world, we?re hell-bent on discovering how bodybuilders can use these supplements to obtain the greatest effect and get the most from all those jaw clenched, teeth-grinding hours spent in the gym. In keeping with this tradition, I?m going to share another first with our loyal customers.

Research in the next few years is going to confirm that inflammation is a critical aspect of building muscle mass. In particular, the ability to reduce inflammation as it goes hand in hand with muscle growth (hypertrophy). As we get older, a chronic inflammatory response manifests within our bodies that makes it increasingly difficult to build and/or maintain muscle as we get older. In directly, this also makes it more difficult to shed body fat.

This increased level of inflammation ultimately results in oxidative damage to our DNA within muscle cells. In particular, the DNA within the mitochondria within each cell. Most of you probably know that the mitochondria are the primary site of ATP (energy) production within cells. This energy comes from the metabolism of all macro-nutrients; fats, carbs and even protein. The mitochondria are the powerhouses in all cells that crank out the seemingly endless supply of energy that powers all processes that keep us alive and allows us to pound out those Max-OT sessions every week.

The bottom line is science has revealed what causes the destruction of your hard earned muscle, therefore, we can start developing therapies to block/reduce this effect. This process is based on nutritional intervention with specific supplements.

The processes that damage muscle DNA and induce inflammation also set the stage for many other highly undesirable conditions such as unwanted weight gain, muscle weakness, type-2 diabetes and heart disease. So we?re talking about research that is going to have an array of benefits for very wide sector of the population.

I?m privy to a lot of this information because I?ve hooked up with some of the worlds finest scientists in this area of research. I'll be working closely with them in the years to come; as part of their research teams and in their laboratories. Now, I?m talking real scientists, not the jack-ass supplement marketers you see in the muscle magazine advertisements wearing lab coats, looking serious while pointing to graphs and charts. Some supplement companies hire people to masquerade as authorities. However, I?m talking incredibly gifted, hard working experts that have published a lot of work in this area.

Now, I can?t let the cat completely out of the bag just yet. It wouldn?t be right. Not all the data is in, and much more work needs to be done. At AST we?re all about facts, not fantasy. This is not a fad. Supplement fads come and go. Remember myostatin-blocking supplements? Weren't they supposed to make bodybuilders huge? Where are they now? How about methoxy or ecdysteone supplements? What happen there?

Back in the real world, natural bodybuilding is going to get very exciting rather soon and one of the reasons is that a clear link between inflammation and muscle loss has been established. How clear is this association?

It?s about as clear as Opera Winfrey?s inability to maintain the same body weight for one week!

That should let you know that this area of research has serious potential.

If you're a bodybuilder that does it drug free, things in the next couple of years are going to get pretty interesting. Rest assured, I'll make sure that it will be you (and your hard work in the gym) that will be the major beneficiary. So, stay loyal, have a fantastic Christmas with your friends and family, and stay tuned! There is much more to come.

[BiggerWeighter]

Skeletal muscle growth requires multiple steps to form large multinucleated muscle cells. Molecules that stimulate muscle growth may be therapeutic for muscle loss associated with aging, injury, or disease. However, few factors are known to increase muscle cell size. We demonstrate that prostaglandin F2{alpha} (PGF2{alpha}) as well as two analogues augment muscle cell size in vitro. This increased myotube size is not due to PGF2{alpha}-enhancing cell fusion that initially forms myotubes, but rather to PGF2{alpha} recruiting the fusion of cells with preexisting multinucleated cells. This growth is mediated through the PGF2{alpha} receptor (FP receptor). As the FP receptor can increase levels of intracellular calcium, the involvement of the calcium-regulated transcription factor nuclear factor of activated T cells (NFAT) in mediating PGF2{alpha}-enhanced cell growth was examined. We show that NFAT is activated by PGF2{alpha}, and the isoform NFATC2 is required for PGF2{alpha}-induced muscle cell growth and nuclear accretion, demonstrating the first intersection between prostaglandin receptor activation and NFAT signaling. Given this novel role for PGF2{alpha} in skeletal muscle cell growth, these studies raise caution that extended use of drugs that inhibit PG production, such as nonsteroidal antiinflammatory drugs, may be deleterious for muscle growth.

[BiggerWeighter]

Modified muscle use or injury can produce a stereotypic inflammatory response in which neutrophils rapidly invade, followed by macro****es. This inflammatory response coincides with muscle repair, regeneration, and growth, which involve activation and proliferation of satellite cells, followed by their terminal differentiation. Recent investigations have begun to explore the relationship between inflammatory cell functions and skeletal muscle injury and repair by using genetically modified animal models, antibody depletions of specific inflammatory cell populations, or expression profiling of inflamed muscle after injury. These studies have contributed to a complex picture in which inflammatory cells promote both injury and repair, through the combined actions of free radicals, growth factors, and chemokines. In this review, recent discoveries concerning the interactions between skeletal muscle and inflammatory cells are presented. New findings clearly show a role for neutrophils in promoting muscle damage soon after muscle injury or modified use. No direct evidence is yet available to show that neutrophils play a beneficial role in muscle repair or regeneration. Macro****es have also been shown capable of promoting muscle damage in vivo and in vitro through the release of free radicals, although other findings indicate that they may also play a role in muscle repair and regeneration through growth factors and cytokine-mediated signaling. However, this role for macro****es in muscle regeneration is still not definitive; other cells present in muscle can also produce the potentially regenerative factors, and it remains to be proven whether macro****e-derived factors are essential for muscle repair or regeneration in vivo. New evidence also shows that muscle cells can release positive and negative regulators of inflammatory cell invasion, and thereby play an active role in modulating the inflammatory process. In particular, muscle-derived nitric oxide can inhibit inflammatory cell invasion of healthy muscle and protect muscle from lysis by inflammatory cells in vivo and in vitro. On the other hand, muscle-derived cytokines can signal for inflammatory cell invasion, at least in vitro. The immediate challenge for advancing our current understanding of the relationships between muscle and inflammatory cells during muscle injury and repair is to place what has been learned in vitro into the complex and dynamic in vivo environment.

skeletal muscle; macro****e; neutrophil; muscle injury; muscle inflammation

[jjohn]

Guys, please don't copy paste something you found somewhere!

[BiggerWeighter]

summarize it or what bro?

[Shortfuze]

The contest is a great idea but I mean...how many different ways can we write about Inflammation? I've already read some awesome info already and its impossible to top that

[shaolinkiwi]

Muscle inflammation is necessary for muscle hypertrophy as humans are not immune to physical damage (although we like to think we at times).

We cannot go to the gym and have an intense workout with some heavy negatives and not be sore, that sore feeling you get after an intense workout is because you damaged skeletal muscle and your bodies own healing factors are regenerating muscle fibres.

It is thought that the events following the initial overloading of skeletal muscle, including inflammation, are necessary for optimal repair and growth of new muscle.

Exercise-induced muscle damage stimulates an inflammatory response; this inflammatory response coincides with muscle repair, regeneration, and growth.

Thus the inflammation response is important to us as bodybuilders because without this response the healing process that occurs during rest would be far less effective, if you lose your power to heal you?re screwed in terms of building muscle.

Muscle inflammation and repair is an essential part of the hypertrophy process, and although you may be sore as hell, the benefits you will reap from the pain are bigger and stronger muscles.

GFH!!

/Rant

[Shortfuze]

This is just a stupid thing I wrote; meant for fun only. The inflammation topic reminded me of the song in "History of the World" by Mel Brooks where he sang the Spanish Inquisition song so I tried to use that

Inflammation! What a pain!
Inflammation! It's insane!
We're on a mission, to rip your tuuuuubes!

By doing so, muscles tear
blood vessels and tissues repair
and you get to be a huge mofo!!

yeah!

[jjohn]

summarize it or what bro?

Well, I want you guys to make some research, and pull what you've understood. Bigger doesn't mean better.

[SHOWTIME]

Inflammation is when you get sore after lifting heavy ass weights becuase everybody wanna be a bodybuilder but ain't nobody want to lift no heavy ass weight. We when ytou get sore from training like an animal that soreness is your body letting you know that is healing, and adpating, so you can get freakin swole!!!

My vote ^^^^^^

[VaughnTrue]

The Role of Macro****es in Muscle Repair and Growth

When resistance exercise involves heavy eccentric muscular contractions (lowering the weight), it is associated with overloading skeletal muscle ?that is, the force requirement of the muscle exceeds what it is accustomed too?and results in injury to skeletal muscle. It has traditionally been felt that the events following the initial injury, including inflammation, are necessary for optimal repair and growth of new muscle. Exercise-induced muscle damage stimulates an acute-phase inflammatory response, which includes infiltration into skeletal muscle by macro****es1. Macro****es (Greek: ?big eaters?) are cells within the tissues that originate from specific white blood cells. One important role of macro****e is the removal of damaged tissue by heavy resistance exercise. Repairing damaged muscle cells is an important function of macro****es in the early stages of muscle damage and inflammation. This inflammatory response coincides with muscle repair, regeneration, and growth, which involves the activation of satellite cells (satellite cell activation is essential for muscle hypertrophy). The number of macro****es per square millimeter of muscle tissue is increased after heavy eccentric exercise compared to concentric exercise (lifting the weight) which may play an important role as to why eccentric contractions produce greater muscle hypertrophy2. Macro****es are also able to promote muscle growth and repair. In vitro studies (test tubes studies) show macro****es can increase muscle cell growth factors3,4, which indicates a role for macro****e-derived factors in muscle growth.

What happens if you suppress your ?Healing Factor??

The healing process that occurs during rest is an important adaptation to building muscle. You may be sore as hell after a heavy leg workout but that means your shocking your muscles into new growth. The inflammatory process although painful for a bodybuilder is an essential part of the muscle growth process. For instance, mediators such as IGF-1 are stimulated by the release of inflammatory cells5. So what happens if you suppress macro****es after injury? Just like Wolverine in the movies, if you lose your ?healing factors? you?re screwed in terms of building muscle. Researchers injected mice with an antibody that reduced macro****e concentrations after a couple of days of muscle overloading (86% reduction in macro****e concentration) and found that muscle fiber repair and growth was significantly impaired after muscle overload6. Macro****e-depletion also reduced muscle regeneration and prevented growth of muscle fibers that normally occurs with muscle overload. These findings suggest that macro****e first invades injured muscle serves to remove cellular debris, after which the subsequent invasive population participates in repair, regeneration and growth.


A strain of mice was recently genetically engineered to test the hypothesis of macro****e invasion to the site of injury is important for muscle regeneration and growth. A strain of mice was bred to be deficient in a protein called MCP-1 (Monocyte chemotactic protein-1), a potent activator for macro****e invasion and inflammation. Researchers damaged muscle fibers of these mice and compared them to normal mice; the mice that had impaired muscle macro****e activity due to a MCP-1 deficiency had impaired muscle regeneration and growth. The researchers speculated that the impaired muscle regeneration was due to macro****es not being able to repair the damaged muscle. Remember, muscle growth takes place during the recovery phase, lifting weights only serves as the stimulus. The research suggests that unless the damaged muscle fiber becomes invaded by macro****es and other repair mediators, it becomes stagnant and muscle repair is halted and the muscle tissue stays damaged. Interestingly, macro****es can increase nitric oxide which expands blood vessels and open up the muscle tissue to blood flow which allows for more macro****es to repair damaged muscle tissue10. NSAIDS Suppress Muscle Growth

You may feel the urge to take an Aleve or Ibuprofen tablet after an intense workout to reduce muscle soreness or you may suffer from a chronic knee or elbow injury from years of heavy lifting but only take NSAIDS when absolutely necessary. According to a new study in Medicine & Science in Sports & Exercise, taking ibuprofen can inhibit muscle hypertrophy. In the study, rats had surgeries performed in which their leg muscles are chronically overloaded to cause muscle hypertrophy. One group of rats received ibuprofen while the other group received nothing. At the end of the study, rats that were administered ibuprofen had a whopping 50% reduction in muscle hypertrophy8. Another study reported that when Non Steroidal Anti-Inflammatory Drugs (NSAIDS) were examined after muscle injury, not only was satellite cell (muscle stem cells) activity in muscle inhibited by their was a increase in myostatin (inhibits muscle growth) production. Examples of NSAIDs include Aspirin, indomethacin (Indocin), ibuprofen (Motrin), naproxen (Naprosyn), piroxicam (Feldene), and nabumetone (Relafen). Recent research suggests that regular use of NSAIDS or COX-2 inhibitors such as Celebrex or Vioxx can significantly reduce muscle hypertrophy by reducing expression of the enzyme COX-2. In conjunction with other research, the COX-2 pathway serves as an important mediator of the inflammation response after exercise serving to repair damaged tissue and is an essential for muscle hypertrophy to occur.

More recent findings have shown cyclooxygenase-2 (COX-2) oral administration of COX-2 inhibitors can slow muscle regeneration and reduce muscle growth after acute injury of muscle7. Interestingly, mice that are genetically engineered to be COX-2 deficient showed less macro****e invasion of injured muscle during regeneration7, which may indicate that macro****es normally promote muscle cell proliferation and muscle regeneration following injury. Alternatively, COX-2 may have a direct effect on muscle cells to affect muscle repair. Additionally, it is well known that in order to build muscle there must be an increase in muscle protein synthesis rates. Studies have reported that if the maximal dosage of ibuprofen or acetaminophen is taken before exercise that protein synthesis rates are blunted9. In that study, subjects performed 10 sets of eccentric exercise performed at 120% of a 1-RM, subjects that received a placebo had average of 76% increase in protein synthesis rates, whereas the subjects whom received either ibuprofen or acetaminophen had no increase in protein synthesis.

In conclusion, don?t take any NSAIDS unless it?s absolutely necessary for alleviating pain. NSAIDS reduce muscle protein synthesis and inhibit muscle hypertrophy. Muscle inflammation and repair is an essential part of hypertrophy process, and although you may be sore as hell, the benefits you will reap from the pain are bigger and stronger muscles.





FTW

[SHOWTIME]

Muscle Inflammation is absolutely necessary to us Bodybuilders, part of the inflammation involves blood rushing to the areas that have been injured, bringing nutrients and oxygen causing swelling at those areas and helping speed up recovery.

At the same time the rebuilding and strengthening process is happening to make the tissue bigger and stronger.

Without inflammation after training we would not be able to heal our muscles that we "injured" and we would be unable to cause the muscles to grow

[Alex08]

i think you need to make the rules a little clearer because apparently almost everyone is just copying and pasting instead of actually cracking a book open or looking at journals to do some research.

[leonidas300]

Damn VT you already ripped off my ripped off post. At least I acknowledged I stole it from Mind and Muscle I charge VT with plagarism and for not responded to my PMs.