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  • Muscle Fiber Hypertrophy vs. Hyperplasia:

    Muscle Fiber Hypertrophy vs. Hyperplasia:
    Has the debate been settled?
    Jose Antonio PhD



    --------------------------------------------------------------------------------
    editors note: One of the fundamental questions in exercise physiology has been the mechanism of muscle adaptation to increased force demands (i.e. strength training). The simple and generally correct answer remains that muscles grow in size due to the growth of existing muscle fibers. However, under extreme conditions of muscle size and workload, there is substantial evidence that muscles can take advantage of a more spectacular mechanism; they can split to form additional new fibers, a mechanism termed hyperplasia. Dr. Antonio has been at the center of this controversial research and did his doctoral work in this area. I think this article is an excellent resource for beginning exercise physiology student and an interesting glimpse into the challenges of physiological research for all. His contribution adds significantly to the teaching value of this site.

    Stephen Seiler



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    WHAT IS HYPERPLASIA?

    Hypertrophy refers to an increase in the size of the cell while hyperplasia refers to an increase in the number of cells or fibers. A single muscle cell is usually called a fiber.

    HOW DO MUSCLE FIBERS ADAPT TO DIFFERENT TYPES OF EXERCISE?

    If you look at a good marathon runner's physique and compared him/her to a bodybuilder it becomes obvious that training specificity has a profound effect. We know that aerobic training results in an increase in mitochondrial volume/density, oxidative enzymes, and capillary density (27). Also, in some elite endurance athletes the trained muscle fibers may actually be smaller than those of a completely untrained person. Bodybuilders and other strength-power athletes, on the other hand, have much larger muscles (14,40). That's their primary adaptation, their muscles get bigger! All the cellular machinery related to aerobic metabolism (i.e., mitochondria, oxidative enzymes, etc.) is not necessary for maximal gains in muscle force producing power, just more contractile protein. We know that this muscle mass increase is due primarily to fiber hypertrophy; that is the growth of individual fibers, but are their situations where muscles also respond by increasing fiber number?

    EVIDENCE FOR HYPERPLASIA

    Scientists have come up with all sorts of methods to study muscle growth in laboratory animals. You might wonder what relevance this has to humans. Keep in mind that some of the procedures which scientists perform on animals simply cannot be done on humans due to ethical and logistical reasons. So the more convincing data supporting hyperplasia emerges from animal studies. Some human studies have also suggested the occurence of muscle fiber hyperplasia. I'll address those studies later.

    DOES STRETCH INDUCE FIBER HYPERPLASIA?

    This animal model was first used by Sola et al. (38) in 1973. In essence, you put a weight on one wing of a bird (usually a chicken or quail) and leave the other wing alone. By putting a weight on one wing (usually equal to 10% of the bird's weight), a weight-induced stretch is imposed on the back muscles. The muscle which is usually examined is the anterior latissimus dorsi or ALD (unlike humans, birds have an anterior and posterior latissimus dorsi). Besides the expected observation that the individual fibers grew under this stress, Sola et al. found that this method of overload resulted in a 16% increase in ALD muscle fiber number. Since the work of Sola, numerous investigators have used this model (1,2,4-8,10,19,26,28,32,43,44). For example, Alway et al. (1) showed that 30 days of chronic stretch (i.e., 30 days with the weight on with NO REST) resulted in a 172% increase in ALD muscle mass and a 52-75% increase in muscle fiber number! Imagine if humans could grow that fast!

    More recently, I performed a study using the same stretch model. In addition, I used a progressive overload scheme whereby the bird was initally loaded with a weight equal to 10% of the its weight followed by increments of 15%, 20%, 25%, and 35% of its weight (5). Each weight increment was interspersed with a 2 day rest. The total number of stretch days was 28. Using this approach produced the greatest gains in muscle mass EVER recorded in an animal or human model of tension-induced overload, up to a 334% increase in muscle mass with up to a 90% increase in fiber number (5,8)! That is pretty impressive training responsiveness for our feathered descendants of dinosaurs.

    But you might ask yourself, what does hanging a weight on a bird have to do with humans who lift weights? So who cares if birds can increase muscle mass by over 300% and fiber number by 90%. Well, you've got a good point. Certainly, nobody out there (that I know of), hangs weights on their arms for 30 days straight or even 30 minutes for that matter. Maybe you should try it and see what happens. This could be a different albeit painful way to "train." But actually the physiologically interesting point is that if presented with an appropriate stimulus, a muscle can produce more fibers! What is an appropriate stimulus? I think it is one that involves subjecting muscle fibers to high tension overload (enough to induce injury) followed by a regenerative period.

    WHAT ABOUT EXERCISE?

    The stretch induced method is a rather artificial stimulus compared to normal muscle activity. What about "normal" muscular exercise? Several scientists have used either rats or cats performing "strength training" to study the role of muscle fiber hyperplasia in muscular growth (9,13,17,18,20-22,25,33,34,39,41,42). Dr. William Gonyea of UT Southwestern Medical Center in Dallas was the first to demonstrate exercised-induced muscle fiber hyperplasia using weight-lifting cats as the model (20,21,22). Cats were trained to perform a wrist flexion exercise with one forelimb against resistance in order to receive a food reward. The non-trained forelimb thus served as a control for comparison. Resistance was increased as the training period progressed. He found that in addition to hypertrophy, the forearm muscle (flexor carpi radialis) of these cats increased fiber number from 9-20%. After examining the training variables that predicted muscle hypertrophy the best, scientists from Dr. Gonyea's laboratory found that lifting speed had the highest correlation to changes in muscle mass (i.e., cats which lifted the weight in a slow and deliberate manner made greater muscle mass gains than cats that lifted ballistically) (33).

    Rats have also been used to study muscle growth (25,39,47). In a model developed by Japanese researchers (39), rats performed a squat exercise in response to an electrical stimulation. They found that fiber number in the plantaris muscle (a plantar flexor muscle on the posterior side of the leg) increased by 14%. Moreover, an interesting observation has been made in hypertrophied muscle which suggests the occurrence of muscle fiber hyperplasia (13, 17, 28, 47). Individual small fibers have been seen frequently in enlarged muscle. Initially, some researchers believed this to be a sign of muscle fiber atrophy. However, it doesn't make any sense for muscle fibers to atrophy while the muscle as a whole hypertrophies. Instead, it seems more sensible to attribute this phenomenon to de novo formation of muscle fibers (i.e., these are newly made fibers). I believe this is another piece of evidence, albeit indirect, which supports the occurrence of muscle fiber hyperplasia.

    EXERCISE-INDUCED GROWTH IN HUMANS

    The main problem with human studies to determine if muscle fiber hyperplasia contributes to muscle hypertrophy is the inability to make direct counts of human muscle fibers. Just the mere chore of counting hundreds of thousands of muscle fibers is enough to make one forget hopes of graduating! For instance, one study determined that the tibialis anterior muscle (on the front of the leg) contains approximately 160,000 fibers! Imagine counting 160,000 fibers (37), for just one muscle! The biceps brachii muscle likely contains 3 or 4 times that number!

    So how do human studies come up with evidence for hyperplasia? Well, it's arrived at in an indirect fashion. For instance, one study showed that elite bodybuilders and powerlifters had arm circumferences 27% greater than normal sedentary controls yet the size (i.e., cross-sectional area) of athlete's muscle fibers (in the triceps brachii muscle) were not different than the control group (47). Nygaard and Neilsen (35) did a cross-sectional study in which they found that swimmers had smaller Type I and IIa fibers in the deltoid muscle when compared to controls despite the fact that the overall size of the deltoid muscle was greater. Larsson and Tesch (29) found that bodybuilders possessed thigh circumference measurements 19% greater than controls yet the average size of their muscle fibers were not different from the controls. Furthermore, Alway et al. (3) compared the biceps brachii muscle in elite male and female bodybuilders. These investigators showed that the cross-sectional area of the biceps muscle was correlated to both fiber area and number. Other studies, on the other hand, have demonstrated that bodybuilders have larger fibers instead of a greater number of fibers when compared to a control population (23,30,36). Some scientists have suggested that the reason many bodybuilders or other athletes have muscle fibers which are the same size (or smaller) versus untrained controls is due to a greater genetic endowment of muscle fibers. That is, they were born with more fibers. If that was true, then the intense training over years and decades performed by elite bodybuilders has produced at best average size fibers. That means, some bodybuilders were born with a bunch of below average size fibers and training enlarged them to average size. I don't know about you, but I'd find that explanation rather tenuous. It would seem more plausible (and scientifically defensible) that the larger muscle mass seen in bodybuilders is due primarily to muscle fiber hypertrophy but also to fiber hyperplasia. So the question that needs to be asked is not whether muscle fiber hyperplasia occurs, but rather under what conditions does it occur. I believe the the scientific evidence shows clearly in animals, and indirectly in humans, that fiber number can increase. Does it occur in every situation where a muscle is enlarging? No. But can it contribute to muscle mass increases? Yes.

    HOW DOES MUCLE FIBER HYPERPLASIA OCCUR?

    There are two primary mechanism in which new fibers can be formed. First, large fibers can split into two or more smaller fibers (i.e., fiber splitting) (6,25,39). Second satellite cells can be activated (11,16,17,43,44).

    Satellite cells are myogenic stem cells which are involved in skeletal muscle regeneration. When you injure, stretch, or severely exercise a muscle fiber, satellite cells are activated (16,43,44). Satellite cells proliferate (i.e., undergo mitosis or cell division) and give rise to new myoblastic cells (i.e., immature muscle cells). These new myoblastic cells can either fuse with an existing muscle fiber causing that fiber to get bigger (i.e., hypertrophy) or these myoblastic cells can fuse with each other to form a new fiber (i.e., hyperplasia).

    ROLE OF MUSCLE FIBER DAMAGE

    There is now convincing evidence which has shown the importance of eccentric contractions in producing muscle hypertrophy (15,24,45,46). It is known that eccentric contractions produces greater injury than concentric or isometric contractions. We also know that if you can induce muscle fiber injury, satellite cells are activated. Both animal and human studies point to the superiority of eccentric contractions in increasing muscle mass (24,45,46). However, in the real world, we don't do pure eccentric, concentric, or isometric contractions. We do a combination of all three. So the main thing to keep in mind when performing an exercise is to allow a controlled descent of the weight being lifted. And on occasion, one could have his/her training partner load more weight than can be lifted concentrically and spot him/her while he/she performs a pure eccentric contraction. This will really put your muscle fibers under a great deal of tension causing microtears and severe delayed-onset muscle soreness. But you need that damage to induce growth. Thus, the repeated process of injuring your fibers (via weight training) followed by a recuperation or regeneration may result in an overcompensation of protein synthesis resulting in a net anabolic effect (12,31).
    "This sport is about extremes - using weights you havent used previously, taking in amounts of food to build greater muscle mass-in amounts you never have done previously, & doing the cardio to keep you at an acceptable offseason training bodyfat that keeps you happy." Dante

    For supplements, visit http://www.trueprotein.com & use this
    DISCOUNT CODE - THA778
    for a 5% Discount
    :wavey:

  • #2
    HAS THE DEBATE BEEN SETTLED?

    In my scientific opinion, this issue has already been settled. Muscle fiber hyperplasia can contribute to whole muscle hypertrophy. There is human as well as rat, cat, and bird data which support this proposition (1-3,5-8,13,17,20-22,25,29,35,37,47), a veritable wild kingdom of evidence. Does muscle fiber hyperplasia occur under all circumstances? No. There are several studies which show no change in fiber number despite significant increases in muscle mass (4,18,19,23,26,30,36,41). Is it possible that certain muscles can increase fiber number more so than others? Maybe. Can any Joe Schmoe off the street who lifts weights to get in better shape increase the number of fibers for instance in their biceps? Probably not. What about the elite bodybuilder who at 5'8" tall is ripped at a body weight of 250 lbs.? Are his large muscles purely the result of muscle fiber hypertrophy? I think it would be extremely naive to think that the massive size attained by elite bodybuilders is due solely to fiber hypertrophy! There is nothing mystical about forming new muscle fibers. Despite the contention that fiber number is constant once you're born (18,19), we now have an abundance of evidence which shows that muscle fiber number can increase. Besides, there is nothing magical at birth which says that now that you're out of the womb, you can no longer make more muscle fibers! A mechanism exists for muscle fiber hyperplasia and there is plenty of reason to believe that it occurs. Of course, the issue is not whether fiber number increases after every training program, stress, or perturbation is imposed upon an animal (or human). The issue is again, under which circumstances is it most likely to occur. For humans, it is my speculation that the average person who lifts weights and increases their muscle mass moderately probably does not induce fiber hyperplasia in their exercised muscle(s). However, the elite bodybuilder who attains the massive muscular development now seen may be the more likely candidate for exercise-induce muscle fiber hyperplasia. If you are interested in a comprehensive scientific treatise on this subject, read a scientific review article that I wrote a few years ago (7).

    KEY TERMS

    anabolic - in reference to muscle, a net increase in muscle protein

    catabolic - in reference to muscle, a net decrease in muscle protein

    concentric - shortening of a muscle during contraction

    eccentric - lengthening of a muscle during contraction

    hyperplasia - increase in cell number

    hypertrophy - increase in cell size

    isometric - no change in muscle length during a contraction

    mitochondria - is an organelle ("little organ") found within cells and is involved in generating ATP via aerobic processes

    muscle fiber - also known as a myofiber; is the multinucleated cell of skeletal muscle

    myoblast - an immature muscle cell containing a single nucleus

    myogenesis - the development of new muscle tissue, esp. its embryonic development

    satellite cell - are the cells responsible in part for the repair of injured fibers, the addition of myonuclei to growing fibers, and for the formation of new muscle fibers.

    REFERENCES

    1. Alway, S. E., P. K. Winchester, M. E. Davis, and W. J. Gonyea. Regionalized adaptations and muscle fiber proliferation in stretch-induced enlargement. J. Appl. Physiol. 66(2): 771-781, 1989.

    2. Alway, S. E., W. J. Gonyea, and M. E. Davis. Muscle fiber formation and fiber hypertrophy during the onset of stretch-overload. Am. J. Physiol. (Cell Physiol.). 259: C92-C102, 1990.

    3. Alway, S.E., W.H. Grumbt, W.J. Gonyea, and J. Stray-Gundersen. Contrasts in muscle and myofibers of elite male and female bodybuilders. J. Appl. Physiol. 67(1): 24-31, 1989.

    4. Antonio, J. and W. J. Gonyea. The role of fiber hypertrophy and hyperplasia in intermittently stretched avian muscle. J. Appl. Physiol. 74(4): 1893-1898, 1993.

    5. Antonio, J. and W.J. Gonyea. Progressive stretch overload of avian muscle results in muscle fiber hypertrophy prior to fiber hyperplasia. J. Appl. Physiol., 75(3): 1263-1271, 1993.

    6. Antonio, J. and W. J. Gonyea. Muscle fiber splitting in stretch-enlarged avian muscle. Med. Sci. Sports Exerc. 26(8): 973-977, 1994.

    7. Antonio, J. and W.J. Gonyea. Skeletal muscle fiber hyperplasia. Med. Sci Sports. Exerc. 25(12): 1333-1345, 1993.

    8. Antonio, J. and W.J. Gonyea. Ring fibers express ventricular myosin in stretch overloaded quail muscle. Acta. Physiol. Scand. 152: 429-430, 1994.

    9. Armstrong, R. B., P. Marum, P. Tullson, and C. W. Saubert. Acute hypertrophic response of skeletal muscle to removal of synergists. J. Appl. Physiol. 46: 835-842, 1979.

    10. Ashmore, C. R. and P. J. Summers. Stretch-induced growth of chicken wing muscles: myofibrillar proliferation. Am. J. Physiol. 51: C93-C97, 1981.

    11. Bischoff, R. Interaction between satellite cells and skeletal muscle fibers. Development. 109: 943-952, 1990.

    12. Carlson, B. M. The regeneration of skeletal muscle. Am. J. Anat. 137: 119-150, 1973.

    13. Chalmers, G.R., R. R. Roy, and V. R. Edgerton. Variation and limitations in fiber enzymatic and size responses in hypertrophied muscle. J. Appl. Physiol. 73(2): 631-641, 1992.

    14. Costill, D. L., E. F. Coyle, W. F. Fink, G. R. Lesmes, and F. A. Witzmann. Adaptations in skeletal muscle following strength training. J. Appl. Physiol. 46(1): 96-99, 1979.

    15. Cote, C., J. A. Simoneau, P. Lagasse, M. Boulay, M. C. Thibault, M. Marcotte, and C. Bouchard. Isokinetic strength training protocols: do they induce skeletal muscle fiber hypertrophy? Arch. Phys. Med. Rehabil. 69: 281-285, 1988.

    16. Darr, K. C. and E. Schultz. Exercise induced satellite cell activation in growing and mature skeletal muscle. J. Appl. Physiol. 63: 1816-1821, 1987.

    17. Giddings, C. J. and W. J. Gonyea. Morphological observations supporting muscle fiber hyperplasia following weight-lifting exercise in cats. Anat. Rec. 233: 178-195, 1992.

    18. Gollnick, P. D., B. F. Timson, R. L. Moore, and M. Riedy. Muscular enlargement and numbers of fibers in skeletal muscles of rats. J. Appl. Physiol. 50: 936-943, 1981. 19. Gollnick, P. D., D. Parsons, M. Riedy, and R. L. Moore. Fiber number and size in overloaded chicken anterior latissimus dorsi muscle. J. Appl. Physiol. 1983; 40: 1292-1297, 1983.

    20. Gonyea, W. J. and G. C. Ericson. An experimental model for the study of exercise-induced muscle hypertrophy. J. Appl. Physiol. 40: 630-633, 1976.

    21. Gonyea, W. J. Role of exercise in inducing increases in skeletal muscle fiber number. J. Appl. Physiol. 48(3): 421-426, 1980.

    22. Gonyea, W. J., D. G. Sale, F. B. Gonyea, and A. Mikesky. Exercise induced increases in muscle fiber number. Eur. J. Appl. Physiol. 55: 137-141, 1986.

    23. Häggmark, T., E. Jansson, and B. Svane. Cross-sectional area of the thigh muscle in man measured by computed tomography. Scand. J. Clin. Lab. Invest. 38: 355-360, 1978.

    24. Hather, B. M., P. A. Tesch, P. Buchanan, and G. A. Dudley. Influence of eccentric actions on skeletal muscle adaptations to resistance training. Acta. Physiol. Scand. 143: 177-185, 1991.

    25. Ho, K. W., R. R. Roy, C. D. Tweedle, W. W. Heusner, W. D. Van Huss, and R. E. Carrow. Skeletal muscle fiber splitting with weight-lifting exercise in rats. Am. J. Anat. 157: 433-440, 1980.

    26. Holly, R. G., J. G. Barnett, C. R. Ashmore, R. G. Taylor, and P. A. Mole. Stretch-induced growth in chicken wing muscles: a new model of stretch hypertrophy. Am. J. Physiol. 238: C62-C71, 1980.

    27. Holloszy, J. O. and F. W. Booth. Biochemical adaptations to endurance exercise in muscle. Rev. Physiol. 273-291, 1976.

    28. Kennedy, J. M., B. R. Eisenberg, S. Kamel, L. J. Sweeney, and R. Zak. Nascent muscle fibers appearance in overloaded chicken slow tonic muscle. Am. J. Anat. 181: 203-205, 1988.

    29. Larsson, L. and P.A. Tesch. Motor unit fibre density in extremely hypertrophied skeletal muscles in man. Eur. J. Appl. Physiol. 55: 130-136, 1986.

    30. MacDougall, J. D., D. G. Sale, S. E. Alway, and J. R. Sutton. Muscle fiber number in biceps brachii in bodybuilders and control subjects. J. Appl. Physiol. 57: 1399-1403, 1984.

    31. MacDougall, J.D. Morphological changes in human skeletal muscle following strength training and immobilization. In: Human Muscle Power (pp. 269-288). N.L. Jones, N. McCartney, A. J. McComas (Eds.). Human Kinetics Publisher, Inc. Champaign, Illinois, 1986.

    32. McCormick, K. M. and E. Schultz. Mechanisms of nascent fiber formation during avian skeletal muscle hypertrophy. Dev. Biol. 150: 319-334, 1992.

    33. Mikesky, A. E., W. Matthews, C. J. Giddings, and W. J. Gonyea. Muscle enlargement and exercise performance in the cat. J. Appl. Sport Sci. Res. 3: 85-92, 1989.

    34. Mikesky, A. E., C. J. Giddings, W. Matthews, and W. J. Gonyea. Changes in muscle fiber size and composition in response to heavy-resistance exercise. Med. Sci. Sports Exerc. 23(9): 1042-1049, 1991.

    35. Nygaard, E. and E. Nielsen. Skeletal muscle fiber capillarisation with extreme endurance training in man. In Eriksson B, Furberg B (Eds). Swimming Medicine IV(vol. 6, pp. 282-293). University Park Press, Baltimore, 1978.

    36. Schantz, P., E. Randall Fox, P. Norgen, and A. Tyden. The relationship between mean muscle fiber area and the muscle cross-sectional area of the thigh in subjects with large differences in thigh girth. Acta Physiol. Scand. 113: 537-539, 1981.

    37. Sjöström, M., J. Lexell, A. Eriksson, and C. C. Taylor. Evidence of fiber hyperplasia in human skeletal muscles from healthy young men? Eur. J. Appl. Physiol. 62: 301-304, 1992.

    38. Sola, O. M., D. L. Christensen, and A. W. Martin. Hypertrophy and hyperplasia of adult chicken anterior latissimus dorsi muscles following stretch with and without denervation. Exp. Neurol. 41: 76-100, 1973.

    39. Tamaki, T., S. Uchiyama, and S. Nakano. A weight-lifting exercise model for inducing hypertrophy in the hindlimb muscles of rats. Med. Sci. Sports Exerc. 24(8): 881-886, 1992.

    40. Tesch, P. A. and L. Larsson. Muscle hypertrophy in bodybuilders. Eur. J. Appl. Physiol. 49: 301-306, 1982.

    41. Timson, B. F., B. K. Bowlin, G. A. Dudenhoeffer, and J. B. George. Fiber number, area and composition of mouse soleus following enlargement. J. Appl. Physiol. 58: 619-624, 1985.

    42. Vaughan, H. S. and G. Goldspink. Fibre number and fibre size in surgically overloaded muscle. J. Anat. 129(2): 293-303, 1979.

    43. Winchester, P. K., M. E. Davis, S. E. Alway, and W. J. Gonyea. Satellite cell activation of the stretch-enlarged anterior latissimus dorsi muscle of the adult quail. Am. J. Physiol. 260: C206-C212, 1991.

    44. Winchester, P. K. and W. J. Gonyea. Regional injury and teminal differentiation of satellite cells in stretched avian slow tonic muscle. Dev. Biol. 151: 459-472, 1992.

    45. Wong, T. S. and F. W. Booth. Protein metabolism in rat gastrocnemius muscle after stimulated chronic concentric exercise. J. Appl. Physiol. 69(5): 1709-1717, 1990.

    46. Wong, T. S. and F. W. Booth. Protein metabolism in rat tibialis anterior muscle after stimulated chronic eccentric exercise. J. Appl. Physiol. 69(5): 1718-1724, 1990.

    47. Yamada, S., N. Buffinger, J. Dimario, and R. C. Strohman. Fibroblast growth factor is stored in fiber extracellular matrix and plays a role in regulating muscle hypertrophy. Med. Sci. Sports Exerc. 21(5): S173-S180, 1989.
    "This sport is about extremes - using weights you havent used previously, taking in amounts of food to build greater muscle mass-in amounts you never have done previously, & doing the cardio to keep you at an acceptable offseason training bodyfat that keeps you happy." Dante

    For supplements, visit http://www.trueprotein.com & use this
    DISCOUNT CODE - THA778
    for a 5% Discount
    :wavey:

    Comment


    • #3
      BigDownUnder, Great info thanx, lots of unanswered questions out there so of my worst ones are muscle cramps and spasms, seems like I read so much stuff that they just have not nailed it down yet, so please if you see any good info on these please shoot them up...
      "That damn log book"

      www.trueprotein.com Highest quality protein at the lowest price...

      Comment


      • #4
        Very good read.
        Anyone can become angry - that is easy, but to be angry with the right
        person, to the right degree, at the right time, for the right purpose,
        and in the right way, that is not easy.
        -- Aristotle (384-322 B.C.)

        Comment


        • #5
          Very interesting indeed, I think you are on to something there! Sounds very logic what you say about the body being able to make more fibers and not only increase in size. At least, I want to believe it is so. LOL

          Comment


          • #6
            Great text, I'm really curious when we'll see the first so called hyperplasia specific training systems

            I bet there will be sth. like this in the future


            So long,
            Grammo
            Never forget to lock your fridge! The INHUMAN one is near!

            Comment


            • #7
              Was a very interesting read, thank you

              Comment


              • #8
                Bump
                International Elite Raw Powerlifter
                Blood - Sweat - Chalk

                Comment


                • #9
                  Another good article on Hyperplasia from abcbodybuilding.com

                  Muscular Density = Hyperplasia!

                  Muscular Hyperplasia is defined as the creation of new muscle fibers. Knowlden (2002) explains:

                  ‘ There are two primary mechanisms in which new fibers can be formed. First large fibers can split into two or more smaller fibers and secondly satellite cells can be activated.



                  Satellite cells are myogenic stem cells, which are involved in skeletal muscle regeneration. When you stretch or intensely work a muscle fiber, satellite cells are activated. Satellite cells can undergo mitosis or cell division and give rise to new myoblastic cells.



                  These immature muscle cells can either fuse with a pre-existing muscle fiber causing that fiber to get bigger (hypertrophy), or these myoblastic cells can fuse with each other to form a new fiber. This is one of the ways to achieve hyperplasia! ‘

                  The application of this principle to bodybuilding is of extreme significance. You see it was long believed that an individual was born with a fixed number of muscle fibers. Density in bodybuilding has been defined as total muscle fibers per unit area. Potential in this sport is directly correlated to this muscle fiber number.

                  Currently evidence from humans, rats, cats and birds suggests that hyperplasia does indeed occur (17, 18, 19, 20, 21, 22, 23)! Some of the more convincing of which has been found by comparing muscle biopsies with elite bodybuilders to that of normal human beings.

                  One study compared the muscle size of strength athletes and normal individuals. The weight training athletes arm's were 27% greater in cross sectional area than the normal, sedentary individuals yet there was no significant difference in the size of their muscles fibers! Thus suggesting that a second mechanism was involved in the increase in overall size of the musculature.

                  Some answer this question by saying that gifted bodybuilders simply were born with more muscle fibers than
                  others. Dr. Antonio who is a leading expert on the subject answers this question, as follows(26):

                  That is, they were born with more fibers. If that was true, then the intense training over years and decades performed by elite bodybuilders has produced at best average size fibers. That means, some bodybuilders were born with a bunch of below average size fibers and training enlarged them to average size. I don't know about you, but I'd find that explanation rather tenuous. It would seem more plausible (and scientifically defensible) that the larger muscle mass seen in bodybuilders is due primarily to muscle fiber hypertrophy but also to fiber hyperplasia....In my scientific opinion, this issue has already been settled. Muscle fiber hyperplasia contributes to whole muscle hypertrophy.

                  Further Nygaard and Nielsen (27) compared the deltoid size of competitive swimmers and normal individuals and found that the deltoid muscles of the swimmers were larger despite smaller muscle fibers! Once again, the swimmers superior size cannot be explained only by an increase in the size of each fibers since their fibers were actually smaller then the sedentary controls. Alway et al. found and concluded that this suggests that adaptations to resistance training may be complex and involve fiber hypertrophy and fiber number (e.g., proliferation). Larsson and Tesch (28) compared the muscle composition of elite bodybuilders with normal standards. Larger cross sectional size was found in the bodybuilders. However, they did not show a superior muscle fiber size compared to sedentary individuals. In fact Tesch concluded that ‘ muscle hyperplasia is one of the adaptation mechanisms of the muscle in the same way as muscle hypertrophy."

                  Another example, is when Alway et al. (19) compared the biceps brachii muscle in elite male and female bodybuilders. A strong correlation in muscle fiber number and cross sectional area was found. It was concluded that the cross-sectional area of the biceps muscle was correlated to both fiber area and number. Hatfield Ph.D. in his book ‘Power: A scientific approach’ is very adamant about the possibility of hyperplasia. Interestingly enough when a poll was taken by the National Strength and Conditioning Association, the majority believed that hyperplasia definitely did contribute to overall muscle growth (29). To comprehend the enormous growth in today's athletes as being purely based on hypertrophy would be a great leap of faith and evidence overwhelmingly points toward hyperplasia being a significant factor in bodybuilding.

                  The Stimulation of HYPERplasia

                  Unfortunately increasing muscular density is a very painful process during a workout and for many days to follow! Studies show that to increase the number of fibers, the participant will have to inflict significant damage to the muscle group (17, 18, 19, 20, 21, 22, 23, 26)! Literally to a point which pushes the envelope of over training. The best way to induce enough micro tears is through an emphasis on eccentric training. The eccentric portion of a repetition has been proven through countless studies to cause the most damage to the target muscle group.

                  5 Eccentric Techniques

                  1. Old School Negatives - These are without a doubt one of the best ways to increase muscular density! Click on the hyperlink to read about them!

                  2. Assisted Negatives - Knowlden suggests the utilization of assisted negatives for hyperplasic processes. These are also a favorite of Lee Priests, which would explain the absolutely insane mass that he has acquired on his quadriceps! Simply lift a weight and have your partner apply pressure on the negative portion of the rep. You need to perform these on machines and or exercises that don't risk trapping you under the weight. For example such a protocol would not be advised on a bench press. However, the technique would be useful on pull-ups and barbell curls. Machines are the safest way to go. If performing leg extensions the participant would lift the weight concentrically unassisted, and then on the eccentric portion have a partner apply excess pressure on the handle handle, while fighting the negative on the way down! This takes advantage of the fact that the athlete can lift more weight on the negative portion of a rep then the positive.

                  3. Heavy Negatives - Here you would get a spotter and use a weight that you could not lift concentrically( positive portion of the rep ) but could use eccentrically( again you can lift heavier on this portion of a rep). I suggest only going 10-15 percent above what you normally can lift for 6 reps. Have your partner assist you on the positive portion of the rep, while you fight the negative!

                  4. Emphasizing the Negative - Again, the key is to literally focus an entire workout on the eccentric portion of a repetition! I would suggest taking 3-5 seconds to lower the weight to incur a maximum amount of damage. And if you attempt to take 10 seconds to lower the weight on a squat you will be destroyed! Normally athletes just take one second to lift a weight and one to two to lower it. In this case you would take much longer. By emphasizing the negative you will increase the micro tears in your muscles. This causes a higher release of satellite cells.

                  5. Forced Negatives: Forced Negatives are performed after you have reached concentric failure. Simply have your partner assist you with the positive rep (taking as much of the weight off as possible ) while you take the negative portion of the rep. Your partner may even apply a bit of pressure( careful, this is dangerous and I only recommend it for intermediate to advanced athletes! )

                  Stretch Overload - Hyperplasia has also been shown to be induced by exercises that enhance the stretch! Examples of these would be preacher curls, weighted sissy squats etc. The key is to employ the one and a half repetition method! If you were to perform a preacher curl, you would perform two reps on the lower half of the exercise. A perfect example of this is shown with Arnold Schwarzenegger's pectorals. He could touch the ground when performing dumbbell flys and I believe he is a clear case of hyperplasia success!

                  Finally, just training insanely (The Austrian Blitz for example!! ) to the point where you are extremely sore the next day will induce an increase in muscular density. Just look at Tom Platz legs. The man trained his lower body harder than anyone in the history of the sport, and I know his legs are not simply the result of hypertrophy! Oliva's forearms are another example, he would perform endless sets of reverse curls with 135 pounds! To the point of exhaustion!

                  17. Alway, S. E., P. K. Winchester, M. E. Davis, and W. J. Gonyea. Regionalized adaptations and muscle fiber proliferation in stretch-induced enlargement. J. Appl. Physiol. 66(2): 771-781, 1989.

                  18. Alway, S. E., W. J. Gonyea, and M. E. Davis. Muscle fiber formation and fiber hypertrophy during the onset of stretch-overload. Am. J. Physiol. (Cell Physiol.). 259: C92-C102, 1990.

                  19. Alway, S.E., W.H. Grumbt, W.J. Gonyea, and J. Stray-Gundersen. Contrasts in muscle and myofibers of elite male and female bodybuilders. J. Appl. Physiol. 67(1): 24-31, 1989.

                  20. Antonio, J. and W. J. Gonyea. The role of fiber hypertrophy and hyperplasia in intermittently stretched avian muscle. J. Appl. Physiol. 74(4): 1893-1898, 1993.

                  21. Antonio, J. and W.J. Gonyea. Progressive stretch overload of avian muscle results in muscle fiber hypertrophy prior to fiber hyperplasia. J. Appl. Physiol., 75(3): 1263-1271, 1993.

                  22. Antonio, J. and W. J. Gonyea. Muscle fiber splitting in stretch-enlarged avian muscle. Med. Sci. Sports Exerc. 26(8): 973-977, 1994.

                  23. Antonio, J. and W.J. Gonyea. Skeletal muscle fiber hyperplasia. Med. Sci Sports. Exerc. 25(12): 1333-1345, 1993.

                  24. Yamada, S., N. Buffinger, J. Dimario, and R. C. Strohman. Fibroblast growth factor is stored in fiber extracellular matrix and plays a role in regulating muscle hypertrophy. Med. Sci. Sports Exerc. 21(5): S173-S180, 1989

                  25. Schantz, P., E. Randall Fox, P. Norgen, and A. Tyden. The relationship between mean muscle fiber area and the muscle cross-sectional area of the thigh in subjects with large differences in thigh girth. Acta Physiol. Scand. 113: 537-539, 1981.

                  26. Antonio, J., Muscle fiber hypertrophy vs. hyperplasia: Has the debate been settled?

                  27. Nygaard E., and Nielsen E., Skeletal muscle fiber capilarisation with extreme endurance training in man. In Eriksson B, Furberg B. Swimming Medicine IV (vol. 6 pp 282-293). University Park Press, Baltimore 1978.

                  28. MacDougall, J.D., D.G. Sale, J.R. Moroz, G.C.B. Elder, J.R. Sutton, and H. Howard. Muscle ultra-structural characteristics of elite power-lifters and bodybuilders. Eur. J. Appl. Physiol. 48:117–126. 1982.

                  29. Craig, Bruce W., 2001: BRIDGING THE GAP: Hyperplasia: Scientific Fact or Fiction?. Strength and Conditioning Journal: Vol. 23, No. 5, pp. 42–44.


                  Pain is weakness leaving the body.


                  :rocker:

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                  • #10
                    Really good read.
                    DOes anyone else have more info on this?
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                    • #11
                      Really interesting read. Bump for more information if anyone has any
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                      • #12
                        Great read. I would like to get more information on this subject also.
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