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Thread: sarcoplasmic vs sarcomere in HST

  1. #1

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    I understand the principles of HST and thats why if you SD you can grow from using submaximal loads...

    My question is whether there is preferential sarcomere growth during the 5's and more sarcoplasmic growth during the 15's?
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  2. #2
    imported_dgunderm Guest

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    The answer lies in what specifically you are stimulating to grow. You obviously couldn't lift the same weight during the 15's as you could during the 5's, so the difference essentially is the type of strain you are putting on your muscle. When you are only doing 5 reps at extremely high weight, you are only putting strain on the contractile proteins that make up the sarcomere, and so you will stimulate sarcomere protein synthesis.

    Sarcoplasmic growth includes organelles like mitochondria that occupy a lot of space. Mitochondria are used when your performance is limited by energy instead of strength. Mitochondria function to feed the sarcomeres with fuel to contract. A set with higher repatitions (and lower weight) is not limited by strength but rather the fuel needed to keep going. This is when you feel your muscles burn. This is the lactic acid in your muscle accumulating due to insufficient rate of fuel production. Increasing mitochondria (sarcoplasmic growth) will enhance performance during the 15's.

    The rep numbers are guidlines of how you are training your muscles, because you can fatigue with any weight; you just may need more or less repatitions to do so. If you fatigue within the first 5 reps then your strength would have been your limiting factor and as result your muscle will produce more contractile proteins to make you stronger. If you fatigue at a high number of reps, it is a result of insufficient energy to the sarcomere from mitochondria and this will stimulate mitochondria production. Fatiguing in between (around 8-12) is thought to be able to stimulate both systems and maximize stimulus of most proteins and therefore maximize hypertrophy.
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  3. #3

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    I understand what your saying dgunderm, but if you selectively favour sarcomere growth by training with heavy weight, then start training with lighter weight stimulating sarcoplasmic growth you can still grow??

    That goes against HST principle of progressive load??

    Also interestingly 8-12 reps have been a consensus for hypertrophy for years, but lyle recommends that 5-8 rep range is perhaps optimal for growth if you had to train within one rep range as you get a good balance of metabolic/ tension work.....



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    Progressive load is important for both types of growth. It is not associated only with sarcoplasmic or only with sarcomere growth.
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    (ratty @ Jul. 08 2009,10:25)
    QUOTE
    I understand what your saying dgunderm, but if you selectively favour sarcomere growth by training with heavy weight, then start training with lighter weight stimulating sarcoplasmic growth you can still grow??

    That goes against HST principle of progressive load??

    Also interestingly 8-12 reps have been a consensus for hypertrophy for years, but lyle recommends that 5-8 rep range is perhaps optimal for growth if you had to train within one rep range as you get a good balance of metabolic/ tension work.....

    My feeling on growth has always been this...

    I can't ever imagine a situation in which, comparing two loads, X, and (X+Y), in which (X+Y) > X, and keeping volume equal, that X would ever result in more overall growth than (X+Y).

    In real world terms, if you compared something like 1 set of 12 reps at like ~70% of your 1 rep max, versus 4 sets of 3 reps at 85%, I don't honestly believe that 12 @ 70% would produce more growth than 4 x 3 @ 85%. *Given the importance of load and, as Dan puts it, time under peak tension, if anything, the latter might actually produce more overall growth imho.

    The rub is this - all else constant, you can usually train with a comparatively lighter load more often than a comparatively heavier load such that our comparison no longer pertains to the real world. *I.e. somebody's joints might only be able to stand 85% of 1 RM loading once or at most twice a week, whereas that same person could train @ 70% three times per week.

    This will screw up comparisons, obviously, because it's not only your muscles recovering from a given session, but your connective tissue and nervous (central and peripheral factors) system as well.
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  6. #6
    imported_dgunderm Guest

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    I understand your example mikeynov, however I disagree that 3 reps will ever result in efficient hypertrophy. You will definately get stronger as your muscles increase sarcomere growth and naturally you would think that if your muscles are increasing the number of sarcomeres then the whole muscle must also get bigger. However new sarcomeres can replace unused mitochondria and therefore the whole muscle may not neccessarily grow in proportion to your increase in strength. Also, if you are going to be doing 4 sets per exercise, it's rather unlikely you would train all muscles in a similar fashion 3 times a week. The concept of HST is that the 3rd and 4th set aren't nearly as effective as the 1st set. So splitting your 4 sets over 3-4 days would be much more effective.

    Ratty, I feel like nobody really addressed your comment. To be honest, I have never thought of starting heavy then going lighter to maximize both systems. I'm assuming you mean within the same workout right? It doesn't really go against progressive load because the next training day you can do the same thing with heavier weights. I spent some time trying to think of any reasons why it wouldn't work but it seems like a reasonable idea. Definately worth a try. The only downside I see is that it would take longer than traditional HST.
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  7. #7

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    (dgunderm @ Jul. 08 2009,5:25)
    QUOTE
    Ratty, I feel like nobody really addressed your comment. *To be honest, I have never thought of starting heavy then going lighter to maximize both systems. *I'm assuming you mean within the same workout right?

    No i dont mean in the same workout, i mean maybe a couple of weeks training heavy and then a couple of weeks training light..

    This as you say would stress the sarcomere and then sarcoplasmic system respectively and both induce growth but completely goes against progressive load?

    Could somebody explain why this could work or why linear progression of load is more optimal???

    And im talking about the mechanisms why...i suspect it could be to do with RBE but not entirely sure....



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    QUOTE
    My question is whether there is preferential sarcomere growth during the 5's and more sarcoplasmic growth during the 15's?


    This article of Dan's should help in answering this question and might be useful to any folks dipping there toes in here. I know I found it helpful in getting a better understanding of this stuff. I'm also pretty sure there are other threads on this subject that you might want to look up.

    QUOTE
    Sarcoplasmic Hypertrophy and Rep Range
    By Dan Moore


    One of the issues I still see when reading training articles is how the rep range dictates whether any hypertrophic response predominantly influences changes in size of the contractile components of muscle cells or the sarcoplasmic volume. The intent of this article is not to dispute that sarcoplasmic hypertrophy exists but to clarify if the rep range used will dictate which protein fraction will increase and whether or not the rep range specifically induces different changes to the nuclear domain of muscle fibers.

    There may very well be other factors such as metabolite accumulation and osmolality shifts within the cell that would give temporary changes to the muscle cell volume and size but since these are mostly temporary I did not feel they should be included in this article.

    What is the Sarcoplasm?
    Within the sarcoplasm there are soluble (or aqueous) components (making up 80 percent of it); composed of ions and soluble macromolecules like enzymes, carbohydrates, different salts and proteins, as well as a great proportion of RNA. This watery component can be more or less gel-like or liquid depending on the condition and the activity phases of the cell. In general, margin regions of the cell are gel-like and the cell's interior is liquid.

    The insoluble constituents of the sarcoplasm are organelles (such as the mitochondria, the chloroplast, lysosomes, peroxysomes, ribosomes), several vacuoles, cytoskeletons as well as complex membrane structures (e.g. sarcoplasmic reticulum).

    The muscle protein fraction that makes up the cytoplasm (sarcoplasm in a muscle cell) is made up of mostly enzymes participating in cell metabolism, such as the anaerobic energy conversion from glycogen to ATP, intracellular transport, and several other enzyme functions. This fraction adds up to about 25 or 30% of the total muscle protein versus the larger and more talked about structural protein (myofibril protein) makes up about 40%.

    Skeletal muscle protein
    When speaking of protein synthesis one of the things that first must be identified is which fraction of protein we are talking about.

    Whole body protein synthesis is an average of the synthesis rates of various proteins in different tissues of the body, skin, muscle, organs, and plasma.

    Mixed muscle protein is an average of the synthesis rates of total muscle proteins and includes mitochondrial, sarcoplasmic, structural components and connective tissue proteins.

    Myofibrillar protein is comprised of individual proteins such as myosin, actin, titin, tropomyosin, troponin, protein C, and some components of mitochondrial proteins.

    Sarcoplasmic proteins are mostly enzymes participating in cell metabolism. However, if the organelles within the muscle cells are broken, this protein fraction may also contain the metabolic enzymes localized inside the sarcoplasmic reticulum, mitochondria and lysosomes.

    Fractional Protein Synthesis
    It has now been known for some time that chronic elevation in protein synthesis above that of breakdown is of prime importance in skeletal muscle hypertrophy (1,2). It is this basis of understanding that we start this article off by looking into how feeding and exercise impacts fractional protein turnover.

    Years ago David Millward and Peter Bates identified that protein synthesis had a direct relationship to both feeding and fasting (3). They also noted that during tissue growth (from feeding) the maintenance of a constant composition necessitates the same absolute increase in synthesis for all proteins, both contractile (myofibril) and soluble (sarcoplasmic). This would mean that the increase in the synthesis rate for each protein will be an increasing proportion of the overall rate for the slower-turning-over proteins or in more simpler terms, the increase of both fractions are held within a ratio.

    Resistance training has shown very strong shifts in protein turnover (4,5) and most of the studies have used mixed muscle protein turnover as the gauge of effectiveness. Unfortunately this method does not show how resistance or dynamic exercise training differently affects each fraction.

    In a study looking at age affects of Protein Synthesis (6) it was noted that by the end of 2 weeks of weight-lifting exercise, MHC and mixed protein synthesis rates increased in both younger and older participants. The actin protein synthesis rate was increased after exercise in only the younger group. The magnitude of the exercise-induced increase in MHC and mixed protein synthesis rates was similar in the younger and older groups. In the younger group, the MHC and Actin (contractile) protein synthesis rate increased 83% and 78% respectively while the mixed muscle protein synthesis rate increased (102%). This study points to the identification that, as with feeding, all proteins are up regulated with resistance exercise. Now the interesting point was that the exercise protocol used seven weight-lifting exercises (Nautilus equipment) that included the chest press, inclined chest press, latissimus pull-down (wide and narrow grip), leg press, knee extension, knee flexion, and two free weight-lifting exercises that included seated overhead press and overhead triceps extension. Each participant completed ten weight-lifting exercise sessions: 2–3 sets/day of the nine exercises listed above, 8–12 repetitions/set, 60–90% of maximum voluntary muscle strength. This was a pretty broad range of intensity and easily points out that the rep range itself isn’t the determining factor.

    To further illustrate that the intensity or rep range utilized does not change this ratio all too dramatically we can look at more recent work looking into the synthetic rates of fractional proteins with dynamic or resistance type exercise.

    Atherton et al. (7) used electrical stimulation with high frequency (HFS; 6x10 repetitions of 3 s-bursts at 100 Hz to mimic resistance training) to identify signalling present during increased protein synthesis. What he noted, significant to this article and discussion, was that HFS significantly increased myofibrillar and sarcoplasmic protein synthesis 3 h after stimulation 5.3 and 2.7 fold, respectively.

    Interestingly Bowtell (8) found that when the same total amount of ATP is turned over, exercise at 60, 75 and 90% of the one-repetition-maximum force results in exactly the same stimulation of muscle protein synthesis, suggesting that once all muscle fibers are recruited increases in tension above 65% cause no further stimulation in muscle protein synthesis. Even though I am not aware if the specific fractions were measured in the Bowtell study it would stand to reason that in light of the previous both fractions would be up-regulated.

    In another study, Louis (9) subjects carried out 20 series of 10 repetitions (with a rest of 80 s after each series) on an isokinetic dynometer to evaluate if Creatine has an impact on anabolic signalling and protein synthesis. Again, in the realm of this article, what was found interesting was that this exercise increased the synthetic rates of myofibrillar and sarcoplasmic proteins by 2- 3 fold.

    Looking at dynamic exercise (one legged kicking), Miller (10) saw that the rates of protein synthesis in the exercised leg increased substantially by 6 h and peaked within 24 h in both myofibrillar and sarcoplasmic fractions, i.e. increases of 2.8 and 2-fold, respectively. The rates of myofibrillar and sarcoplasmic protein synthesis in the exercised muscle had fallen slightly by 48 h but were still significantly above the rates in the rested leg. By 72 h, the rates of both fractions had decreased.

    Our last look at fractional elevations will look at whether or not there is a fiber type dependency. In many animals the rate of protein synthesis is higher in slow-twitch, oxidative than fast-twitch, glycolytic muscles. To find if this held true for muscles in the human body a recent study (11) recruited nine healthy, young men and with a constant infusion looked at synthetic rates in the soleus, vastus lateralis and tricep. Type-1 fibers contributed 83 +/- 4% (mean +/-s.e.m.) of total fibers in soleus, 59 +/- 3% in vastus lateralis and 22 +/- 2% in triceps. The basal myofibrillar and sarcoplasmic protein fractional synthetic rates (FSR, % h(-1)) were 0.034 +/- 0.001 and 0.064 +/- 0.001 (soleus), 0.031 +/- 0.001 and 0.060 +/- 0.001 (vastus), and 0.027 +/- 0.001 and 0.055 +/- 0.001 (triceps). During amino acid infusion, myofibrillar protein FSR increased to 3-fold, and sarcoplasmic to 2-fold above basal values (P < 0.001), again showing that even within differing types of muscle tissue the ratio remains.

    What can be seen when reviewing these and many other papers on the subject is the response to resistance training of fractional elevation remains in line with the results of feeding, both are elevated but the slower turnover proteins (myofibrillar) generally show a larger magnitude in increase. Since these studies show that this holds true with resistance training, dynamic exercise and HFES, all utilizing differing intensities and work output, it seems unlikely that the rep range is the sole cause of any increase in sarcoplasmic fraction up-regulation.

    Nuclear Domains
    It is well established that satellite cell contribution is a very important factor in muscle hypertrophy (12,13). As a cell grows and increases it’s cytoplasmic volume, the nucleus must maintain mRNA production for the entire area of increased size of cytoplasm (14). Since muscle cells are multi-nucleic, each nucleus controls mRNA over a finite area or its domain (14,15), hence the term nuclear domain.
    Skeletal muscle hypertrophy has shown to induce increases in myonuclei and or increases in domain size (16). Resistance training has reported a very broad range of increases in fiber hypertrophy (17). In several hypertrophy studies it appears that there is a limit that needs to be reached before domain size increases necessitates increased nuclei donation. Studies that have shown significant increase in hypertrophy, above 26%, also showed large additions of myonuclei in animals (18-20) and in humans (21).

    Work in humans is rather limited but what can be seen in this smaller body of work is very interesting. Acutely, resistance training and resistance type training do not exert the same magnitude of response in humans as what is seen in smaller animals.

    A recent study (22) examining the acute effect of training showed less significant changes in donated nuclei and in fact after an acute bout of (a) fifty one-legged ‘drop-down’ jumps were performed from a stable platform of 45 cm, (b) eight sets of ten maximal eccentric knee extensions at –30 degree/s using an isokinetic dynamometer and ( c) eight sets of ten maximal eccentric knee extensions at –180 degree/s using an isokinetic dynamometer, satellite cell proliferation did occur but there was no increased satellite cell donation. Apparently a single bout in humans is not enough to induce the same changes seen in smaller animals.

    Kadi looked at chronic application in a very interesting and telling look at training and detraining. (23). In this study he subjected 15 subjects to 3 months of progressive resistance training using a 6-12 RM. The various exercises were conducted in 4–5 sets, in the first weeks (training sessions 0–5) exercises involved 10–12 RM loads, followed by 10 RM loads in early weeks (training sessions 6–15), heavier loads of 6–10 RM in the later weeks (training sessions 16–30), and very heavy loads of 6–8 RM in the final weeks (training sessions 31–38). The subjects then detrained for 3 months. Satellite cell activity increased significantly over the entire training period. Reaching significance at around 30 and again at the 90-day marks. Hypertrophy of fiber increased at 30 days and 90 days, 6.7% and 17% respectively. Interestingly though was the observation that the area controlled by each nuclei was virtually unchanged over the entire training period. This clearly illustrates that the rep range was not the primary inducer of hypertrophy or domain volume changes since the fiber size and satellite cell count increased no matter the rep range. It also clearly indicates that the duration of chronic training is a key element in both hypertrophy and satellite cell activity.

    An earlier study by the same researcher (24) saw a concomitant increase in satellite cell count and an increase in myonuclei donation over a 10-week training protocol in female athletes. The muscle examined in this study was the trapezius so it could be that the increase could be muscle specific, as it’s been shown that the trapezius has a higher androgen receptor content (25). This may have also been another reason why the previously cited work by Kadi showed such a difference as the biopsies were taken from the vastus lateralis.

    In summary it is very common to see studies reflecting both increased protein synthesis and hypertrophy with a myriad of rep ranges and resistance training protocols. The extent of hypertrophy may be a direct reflection in increased translational efficiency or an increase in pre-translational abundance of mRNA. The differences may be owing to the training status of the individual and not necessarily the rep range used in the resistance training routine. Although it appears that the rep range will have an impact on metabolic shifts in isoform content, this does not change the sarcoplasmic vs. contractile protein synthesis ratio but merely dictates which fiber type will experience the greater amount of hypertrophy.

    As stated in Rennie’s 2004 review (26), it may take 20 weeks of resistance training to increase hypertrophy by 20%. This coincides very well with the research presented in this article, as it appears that the change in fiber size has a direct correlation to when satellite cells donate their nuclei for continued domain regulation. Therefore moderate increases in nuclear domain are very possible without the aided donation of nuclei from satellite cells and this does not appear to be rep range dependant. A statement can also be made that the results seen in small animals and humans may be very different. This may be owing to the extent of damage that is seen and how hypertrophy and necrotic damage stimulate the satellite pool differently but that is beyond the scope of this article.

    Dan Moore *
    Hypertrophy-Research.com


    (1)Changes in rates of protein synthesis breakdown during hypertrophy of the anterior and posterior latissimus dorsi muscles. Biochem. J. 176:407–17

    (2)Protein turnover during skeletal muscle hypertrophy.Fed. Proc. 39:42–47

    (3)Synthesis rates of myofibrillar and sarcoplasmic protein fractions in different muscles and the changes observed during postnatal development and in response to feeding and starvation Biochem. J. (1983) 214,587-592

    (4)Increased rates of muscle protein turnover and amino acid transport after resistance exercise in humans. Am J Physiol Endocrinol Metab 268: E514–E520, 1995.

    (5)Changes in human muscle protein synthesis following resistance exercise. J Appl Physiol 73: 1383–1388,1992.

    (6)Resistance exercise acutely increases MHC and mixed muscle protein synthesis rates in 78–84 and 23–32 yr olds Am J Physiol Endocrinol Metab 278: E620–E626, 2000.

    (7) Selective activation of AMPK-PGC-1alpha or PKB-TSC2-mTOR signaling can explain specific adaptive responses to endurance or resistance training-like electrical muscle stimulation. FASEB J. 2005 May;19(7):786-8. Epub 2005 Feb 16.

    (8) Stimulation of human quadriceps protein synthesis after strenuous exercise: no effects of varying intensity between 60 and 90% of one repetition maximum (1RM). J Physiol 547.P, P16.

    (9) No effect of creatine supplementation on human myofibrillar and sarcoplasmic protein synthesis after resistance exercise. Am J Physiol Endocrinol Metab. 2003 Nov;285(5):E1089-94.

    (10)Coordinated collagen and muscle protein synthesis in human patella tendon and quadriceps muscle after exercise.J Physiol. 2005 Sep 15;567(Pt 3):1021-33.

    (11)Protein synthesis rates in human muscles: neither anatomical location nor fibre-type composition are major determinants. J Physiol. 2005 Feb 15;563(Pt 1):203-11. Epub 2004 Dec 20.

    (12)Gamma irradiation prevents compensatory hypertrophy of overloaded mouse extensor digitorum longus muscle. J. Appl. Physiol. 73:2538–43

    (13)Cellular molecular responses to increased skeletal muscle loading after irradiation. Am. J. Physiol.
    Cell Physiol. 283:C1182–95

    (14)The control of cell mass and replication. The DNA unit-a personal 20 year study. Early Hum Dev 12, 211-239.

    (15) Nuclear Domains in Muscle Cells. Cell 59, 771-772

    (16)Regulation of Skeletal muscle fiber size, shape and function. J Biochem (Suppl. 1), 123-133

    (17) Exercise, protein metabolism, and muscle growth. Int J Sport Nutr Exerc Metab. 2001 Mar;11(1):109-32. Review.

    (18)Morphometric analyses on the muscles of exercise trained and untrained dogs. Am J Anat. 1983 Mar;166(3):359-68.

    (19)Plasticity of myonuclear number in hypertrophied and atrophied mammalian skeletal muscle fibers. J Appl Physiol. 1995 May;78(5):1969-76.

    (20)Modulation of myonuclear number in functionally overloaded and exercised rat plantaris fibers.J Appl Physiol. 1999 Aug;87(2):634-42.

    (21)Is Hypertrophy limited in elderly muscle fibers? A comparison in elderly and young strength-trained men. Basic Appl Myol 1998; 8, 419-427

    (22)Changes in satellite cells in human skeletal muscle after a single bout of high intensity exercise. J Physiol. 2004 Jul 1;558(Pt 1):333-40. *

    (23)The effects of heavy resistance training and detraining on satellite cells in human skeletal muscles. J Physiol. 2004 Aug 1;558(Pt 3):1005-12.

    (24)Concomitant increases in myonuclear and satellite cell content in female trapezius muscle following strength training. Histochem Cell Biol 2000; 113, 99-103.

    (25)The expression of androgen receptors in human neck and limb muscles: effects of training and self-administration of androgenic-anabolic steroids. Histochem Cell Biol. 2000 Jan;113(1):25-9.

    (26)Control of the Size of the Human Muscle Mass Annu. Rev. Physiol. 2004. 66:799–828
    "Be the best that you can be."

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  9. #9
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    QUOTE
    i mean maybe a couple of weeks training heavy and then a couple of weeks training light..

    I think this will work as long as you are increasing load over time and as long as you have a reset/deload/SD week or two every so often (maybe every 8-12 weeks).

    If you take, for example, a training program where there are two weeks training at ~70-80% 1RM followed by two weeks training at ~90-95 1RM, what you have, in effect, are four week cycles of load progression. If you were to ensure that you increased loading for each of these short four week cycles, then over time you are increasing load on the bar. Eventually you will stall out and have to SD (or whatever you want to call it) and then start over.

    What would be interesting is finding whether there are any benefits at all to be had from training this way over a regular load progression. So, does a sudden jump to heavy loads every two weeks (effectively a large increment in loading) and then maintaining (or increasing) those heavy loads for two weeks cause a larger PS response (on average) than for a regular progression using the same amount of work? I don't know (but I doubt it).

    What you might find is that dropping back down to lighter loads following heavy work, and without SD, produces very little PS response unless you are pushing close to failure for much of the time (to get full fibre recruitment). If this was the case then you would effectively be deloading for two weeks and, I suspect, inducing very little to no PS response over that time before bumping up the loads again for a stronger PS response during the two weeks of heavy work. If you spent the two light weeks working close to failure, you would be entering the heavy weeks with your CNS in a fatigued state right form the start. This might well prevent you from increasing the loads as much as you could have if you were carrying less fatigue during the heavy weeks.

    At any rate, as long as the load on the bar is going up over time then you are either getting some growth (if your diet and cal intake is in order) or you are putting yourself in a position where growth can occur because your strength has increased. Would this be a more or less efficient way to train for hypertrophy as compared to a regular cycle of steadily increasing loading? Could you progress loads more quickly over time? Again, I doubt it, but I don't know.

    If you try this as an experiment, it would be interesting if you log your workouts and your results (plus diet).
    "Be the best that you can be."

    PR's:
    Deadlift: 215kg (474lb) - pre-hernia!
    Low-bar Back Squat: 190kg (419lb) 16/04/10 @BW ~210lb
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    Total: 1,180lb
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    (Lol @ Jul. 09 2009,5:25)
    QUOTE
    I know I found it helpful in getting a better understanding of this stuff.

    Dan
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