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    www.abcbodybuilding.com Muscle Physiology 1

    Physiological Aspects of Physique Building Part 1

    Researched and Composed by Jacob Wilson, BSc. (Hons), MSc. CSCS

    AbstractThe purpose of this paper was to review the topic of maximized muscular

    hypertrophy within the bodybuilding regimen. Muscular hypertrophy is defined as anincrease in diameter of muscular tissue.

    Hypertrophy - Muscular GrowthHypertrophy is the result of an increase in the contractile filaments, which comprise

    a muscle fiber. Of prime importance are the actin and myosin filaments within amyofibril. These allow for the expression of musculature contraction. Adaptations

    within these structures are a consequence of contractile demands on the systemitself. The increase seen can be viewed grossly through two mechanisms. The first

    adaptation concerns the addition of myofilaments to the peripheral or outer region ofthe myofibril, resulting in greater overall fiber diameter. The second adaptation is

    accomplished through myofibrillar hyperplasia, in that the actual number of

    myofibrils within a muscle fiber increase (14, 15,). The majority of a muscle fiber ismade up of these myofibrils. Therefore increasing their size and number will result

    in enhanced cross sectional area.

    It should be clearly understood that resistance training increases protein synthesisfor up to 24 hours post exercise (16). Protein synthesis is the process by which DNA

    encodes for the production of amino acids and proteins. The process of anabolism inregards to contractile tissue is literally heightened, resulting in a super compensation

    effect (an effect which raises structural and contractile tissue to above pre trainingbout levels). Amino acids are the building blocks of the proteins, which comprise the

    musculature. An amino acid is characterized by a nitrogen containing group, an acidgroup, and a variable group. The latter of which can take on 20 different

    combinations. It is for this reason that a sufficient protein intake is vital to

    increasing muscular size. That is, a diet rich in amino acids must be supplied inorder to augment the supercompensatory process previously described.

    Why Moderate Reps Stimulate Optimal Hypertrophy

    Evidence suggests that moderate repetition sets provide an optimal stimulus forgrowth in the fast twitch fibers, while high repetition sets may optimize the

    hypertrophy process in slower twitch fibers. Reasons follow. First, sets which fallwithin a 1 to 5 repetition continuum will most likely cause the participant to fail due

    to neurological signaling problems before an optimal stimulus for muscle growth can

    be induced (1, 2). Secondly moderate repetition sets (6-12) take full advantage of

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    human recruiting systems. In general, the nervous system will recruit lower

    threshold fibers first and enlist high threshold fibers progressively as the set

    continues on. By the end of a set all available muscle cells have been brought intoplay (3). Thirdly the release of anabolic hormones is highest after these types of

    sets (4, 5, 6, 7, 8).

    A greater circulation of anabolic hormones in the body, results in greater adaptationsto imposed demands. Interestingly enough, much evidence supports the postulatethat lactic acid production can be very conducive to the release of hormones such as

    testosterone and growth hormone ( 3, 4, 5 ). Lactic acid is a by-product of glycolysis

    (6). This is the energy system that is used most heavily during 30-90 seconds ofwork. Glycolysis is directed by a series of enzymes, which comprise what is known

    as a chemical pathway. The enzyme lactate dehydrogenase is more active than anyenzyme in the pathway. Therefore the more the participant relies on this pathway,

    the greater the build up of lactate will be. Hakkinen et al. found that blood lactateconcentration during exercise correlated significantly (P < 0.01) with the increase in

    serum GH concentration. While Lu et al. in the Journal of Sports medicine found that

    increased plasma testosterone levels in males during exercise is at least partially aresult of a direct stimulatory effect of lactate on the secretion of testosterone by

    increasing testicular cAMP production. Consequently blood lactate levels rise highestin moderate sets, with moderate rest. As opposed to low repetition, relatively high

    rest sets.

    Power lifting type movements have a greater reliance on the creatine phosphate (PC)

    system, which is used for, extremely low repetition, high intensity sets. Note that

    intensity in this light is in reference to percentage of the athletes one repetitionmaximum. The PC system does not result in lactic acid production and as a result is

    frequently referred to as the A Lactic anaerobic system.

    Further moderate repetition sets augment the blood pump phenomena. The benefits

    of which are numerous. For example, this phenomenon can facilitate myofibrillar

    hydration ( 9 ). A pump results through the collapsing of veins. These vessels carryblood away from the muscle tissue, while arteries act to deliver the blood. As veins

    begin to fail, the arteries continue to bring blood to the muscles. The resulting buildup of fluid causes a flow of blood to go back into the musculature. Such an increase

    in fluid super hydrates the tissue. A process, which can lead to the inhibition ofprotein catabolism, and the augmentation of protein anabolism or synthetic rates

    (10, 11, 12). In a review on cellular hydration, Waldegger et al. (12) states that the paramount importance of cell volume for the regulation of cell function, including

    protein metabolism, has been recognized. The results of their research yielded the

    following results:

    cell swelling inhibits proteolysis

    cell swelling stimulates protein synthesis

    cell shrinkage stimulates proteolysis

    cell shrinkage inhibits protein synthesis

    Haussinger suggests that the degree of cellular hydration is not only a major

    determinant of cellular protein and RNA turnover, but also that hormones and amino

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    acids can modify protein turnover by altering the hydration state of the cell. He

    concludes that cell swelling triggers an anabolic, proliferative pattern of

    metabolism, whereas cell shrinkage is a catabolic and antiproliferative signal. Further, blood is responsible for the delivery of nutrients needed for protein

    metabolism.

    Finally time under tension has been a proven factor in stimulating optimal growth(13). Contraction resulting from actin and myosin filamentous interaction, which willlead to damage of both the cytoskeleton and contractile units. The time under

    tension during lower repetition sets appears to be suboptimal for the hypertrophy

    sought stimulus.

    Various Training Methodologies Between Various Regions of The Body

    Knowing how to stimulate hypertrophy in type I, IIA and IIB fibers is half the battle.The other half is understanding how to apply these concepts to each individual body

    part. An understanding of the fact that each muscle group is made up of specificfiber compositions will augment this process. For example, if a muscle is 86 percent

    fast twitch, working the slow twitch fibers to a heightened extent would underminethe participants training efficiency. Further, if a muscle is predominantly slow twitchand the participant ignores this make up, then hypertrophy will be hindered. The

    following will provide a guide on how to target various musculature:

    1. Always hit the fast twitch cells, even if the muscle group is pre-dominantly slowtwitch. The reason is due to the relatively larger size of this particular fiber. What

    will not occur is an overly dominant fast twitch workout.

    2. If a muscle group is dominated by a slow twitch makeup, the participant will need

    to dedicate significant time to stimulating growth in these cells. A recommendationwould include a few medium range sets to target the small percentage of fast twitch

    fibers, followed by a regimen, which blasts the higher percentage cells to bits for the

    majority of the workout by using a higher repetition scheme.

    3. If a muscle group has an even makeup, the majority of time should be spent

    working the fast twitch fibers due to their size. However, time should still bedelineated to the slow twitch fibers. You should switch around the ratios as well.

    Lets say a muscle group is 50 / 50. Then Spend 60-70 percent of the time on fasttwitch with the remainder of time on the remaining fibers. Occasionally for a burst of

    growth, emphasize the type I cells 50-80 percent of the time. This should be used

    sparingly, but certainly of prime importance.

    4. If a muscle group such as the hamstrings are dominantly fast twitch (70-80

    percent) then spend about 80-90 percent of the time on fast twitch fibers, and 10-20

    percent of the time on the slower fibers. Perhaps just one burn out / high repetitionset at the end of the workout.

    Note: Muscle Fiber Ratios are provided in the Anatomy Section of the Site

    Muscular Density = Hyperplasia!

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    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 largefibers 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 areactivated. 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 causingthat 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 doesindeed 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 ofnormal human beings.

    One study compared the muscle size of strength athletes and normal individuals. Theweight training athletes arm's were 27% greater in cross sectional area than thenormal, sedentary individuals yet there was no significant difference in the size of

    their muscles fibers! Thus suggesting that a second mechanism was involved in theincrease in overall size of the musculature.

    Some answer this question by saying that gifted bodybuilders simply were born with

    more muscle fibers thanothers. 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 bestaverage size fibers. That means, some bodybuilders were born with a bunch of belowaverage 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 (andscientifically defensible) that the larger muscle mass seen in bodybuilders is due

    primarily to muscle fiber hypertrophy but also to fiber hyperplasia....In my scientificopinion, this issue has already been settled. Muscle fiber hyperplasia contributes to

    whole muscle hypertrophy.

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    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 swimmerssuperior size cannot be explained only by an increase in the size of each fibers since

    their fibers were actually s m a l l e r then the sedentary controls. Alway et al. foundand 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 sedentaryindividuals. 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 andcross 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 ofhyperplasia. Interestingly enough when a poll was taken by the National Strength

    and Conditioning Association, the majority believed that hyperplasia definitely didcontribute 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 faithand 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 workoutand 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 eccentrictraining. The eccentric portion of a repetition has been proven through countlessstudies 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 forhyperplasic 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. Youneed to perform these on machines and or exercises that don't risk trapping youunder 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 participantwould lift the weight concentrically unassisted, and then on the eccentric portion

    have a partner apply excess pressure on the handle handle, while fighting thenegative 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.

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    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 percentabove 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 workouton the eccentric portion of a repetition! I would suggest taking 3-5 seconds to lowerthe 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 wouldtake 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 (takingas 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 wereto 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'spectorals. 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 whereyou 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 inthe 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 setsof reverse curls with 135 pounds! To the point of exhaustion!

    To add I would not suggest training for hyperplasia every workout. Or at least not

    for everybody part. Perhaps pick one body part to destroy a week and train yourothers normally.

    Jacob [email protected]

    President Abcbodybuilding

    References and Sources Cited

    1. Zehr, E.P. Ballistic movement: Muscle activation and neuromuscular adaptation.

    Can. J. Appl. Physiol.19:(4)363378. 1994.

    3. Schoenfeld, Brad, 2000: Repetitions and Muscle Hypertrophy. Strength andConditioning Journal: Vol. 22, No. 6, pp. 6769.

  • 7/22/2019 physiologicalaspectsofphysiquebuilding.pdf

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    www.abcbodybuilding.com Muscle Physiology 7

    4. 8. Kraemer, W.J. Changes in hormonal concentrations after different heavy-

    resistance exercise protocols in women.J. Appl. Physiol.75:(2)594604. 1993.

    5. Lu, S.S. Lactate and the effects of exercise on testosterone secretion: Evidencefor the involvement of a cAMP-mediated mechanism. Med. Sci. Sports Exerc.

    29:(8)10481054. 1997

    6. 4.Dudley GA (1988) Metabolic consequences of resistive-type exercise. Med Sci

    Sports Exerc.20(5 Suppl):S158-S161

    7. Kraemer, W.J. Hormonal and growth factor responses to heavy resistance exerciseprotocols.J. Appl. Physiol.69:(4)14421450. 1990.

    8. 7. Kraemer, W.J. Endogenous anabolic hormonal and growth factor responses to

    heavy resistance exercise in males and females. Int. J. Sports Med.12:(2)228235.1991.

    9. Wilmore, J.H. Physiology of Sport and Exercise.(2nd ed.). Champaign, IL: Human

    Kinetics, 1999.

    10. 4. Hussinger, D. Cellular hydration state: An important determinant of protein

    catabolism in health and disease. Lancet.341:(8856)13301332. 1993.

    11. Millar, I.D. Mammary protein synthesis is acutely regulated by the cellularhydration state. Biochem. Biophys. Res. Commun.230:(2)351355. 1997.

    12. Waldegger, S. Effect of cellular hydration on protein metabolism. Miner.Electrolyte Metab.23:(36)201205. 1997

    13. Evans, W.J. The metabolic effects of exercise-induced muscle damage. Exerc.

    Sport Sci. Rev.19: (-HD-). 99125. 1991.

    14. Conroy, B.P. and R.W. EarleBone , muscle, and connective tissu adaptations to

    pjysical activity. In essentials of Strength Trianing and Conditioning. T. R. Baechle.ed. Champaign, Il; Human Kinetics, 1994.

    15. Tesch, P.A. Skeletal muscle adaptations consequent to long term heavy

    resistance exercise Med. Sci. Sports Exerc. 20:S132-S134. 1988

    16. Staribm R,S,, D.L. Karapondo, W.J. Kraemer, A.C. Fry, S.E. Gordon, J.E. Falkel,

    F.C. Hagerman, and R.S. Hikida. Skeletal muscle adaptations during early phase of

    heavy-resistance training in men and woman. J Appl. Physiol. 76:1247-1255. 1994

    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.

  • 7/22/2019 physiologicalaspectsofphysiquebuilding.pdf

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    www.abcbodybuilding.com Muscle Physiology 8

    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 musclehypertrophy. 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 subjectswith large differences in thigh girth. Acta Physiol. Scand. 113: 537-539, 1981.

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

    27. Nygaard E., and Nielsen E., Skeletal muscle fiber capilarisation with extremeendurance 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.48:117126. 1982.

    29. Craig, Bruce W., 2001: BRIDGING THE GAP: Hyperplasia: Scientific Fact or

    Fiction?. Strength and Conditioning Journal: Vol. 23, No. 5, pp. 4244.

    30. Target Bodybuilding

    31. Barnett, C., V. Kippers, and P. Turner. Effects of variations of the bench press

    exercise on the EMG activity of five shoulder muscles.J. Strength Cond. Res.9:222227. 1995.

    32. Brown, J.M.M., C. Solomon, and M. Paton. Further evidence of functional

    differentiation within biceps brachii. Electromyogr. Clin. Neurophysiol.33:301309.1993.

    33. 29. Glass, S.C., and T. Armstrong. Electromyographical activity of the pectoralismuscle during decline bench presses.J. Strength Cond. Res.11:163167. 1997.

  • 7/22/2019 physiologicalaspectsofphysiquebuilding.pdf

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    www.abcbodybuilding.com Muscle Physiology 9

    34. Sarti, M.A., M. Monfort, M.A. Fuster, and L.A. Villaplana. Muscle activity in upper

    and lower rectus abdominus during abdominal exercises.Arch. Phys. Med. Rehabil.

    77:12931297. 1996.

    35. Lipetz, S., and B. Gutin. An electromyographic study of four abdominal

    exercises. Med. Sci. Sports 2:35-38. 1970.

    37. Kawakami, Y., T. Abe, S.-Y. Kuno, and T. Fukunaga. Training-induced changes

    in muscle architecture and specific tension. Eur. J. Appl. Physiol. 72:37-43 1995.

    38. 4.Kawakami, Y., T. Abe, S.-Y. Kuno, and T. Fukunaga. Training-induced changesin muscle architecture and specific tension. Eur. J. Appl. Physiol. 72:37-43 1995.

    39. ANTONIO, JOSE, 2000: Nonuniform Response of Skeletal Muscle to HeavyResistance Training: Can Bodybuilders Induce Regional Muscle Hypertrophy?. The Journal

    of Strength and Conditioning Research: Vol. 14, No. 1, pp. 102113.

    40. Elder, G.C.B., K. Bradbury, and R. Roberts. Variability of fiber type distributions

    within human muscles.J. Appl. Physiol.53:14731480. 1982.

    41. Punkt, K., H. Mehlhorn, and H. Hilbig. Region- and age-dependent variations ofmuscle fiber properties.Acta Histochem.100:3758. 1998.

    42. Sola, O.M., S. Herring, G. Zhang, X. Huang, N. Hayashida, L.C. Haines, R.Thomas, B.A. Kakulas, and L.R. Sauvage. Significance of the biopsy site of the

    latissimus dorsi muscle for fiber typing.J. Heart Transplant.11:S315S319. 1992.

    44. Johnson, M.A., Polgar, J., Weightman, D. & Appleton, D. (1973). Data on thedistribution of fibre types in thirty-six human muscles: An autopsy study. Journal of

    the Neurological Sciences, 18, 111 - 129.

    45. ('Muscle Function after Exercise-Induced Muscle Damage and Rapid Adaptation,'

    Medicine and Science in Sports and Exercise, vol. 24(5), pp. 512-520, 1992)

    46. Differences in Skeletal Muscles,' Journal of Applied Physiology, vol. 85(1), pp.

    98-104, 1998)

    47. Antonio, J., and W.J. Gonyea. Ring fibres express ventricular myosin in stretchoverloaded quail muscle.Acta Physiol. Scand.152:429430. 1994.

    48. Andersen, J.L., H. Klitgaard, and B. Saltin. Myosin heavy chain isoforms in single

    fibres from m. vastus lateralis of sprinters: Influence of training.Acta Physiol. Scand.

    151:135142. 1994.

    49. Klitgaard, H., M. Zhou, and E.A. Richter. Myosin heavy chain composition of

    single fibers from m. biceps brachii of male body builders.Acta Physiol. Scand.140:175180. 1990.

    50. Sakuma, K., A. Yamaguchi, and S. Katsuta. Are region-specific changes in fibretypes attributable to nonuniform muscle hypertrophy by overloading?. Eur. J. Appl.

    Physiol.71:499504. 1995.

  • 7/22/2019 physiologicalaspectsofphysiquebuilding.pdf

    10/10

    www.abcbodybuilding.com Muscle Physiology 10

    51. Alway, S.E. Stretch induces non-uniform isomyosin expression in the quail

    anterior latissimus dorsi muscle.Anat. Rec.237:17. 1993

    52. Alway, S.E., W.H. Grumbt, J. Stray-Gundersen, and W.J. Gonyea. Effects ofresistance training on elbow flexors of highly competitive bodybuilders.J. Appl.

    Physiol.72:15121521. 1992

    53. 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.66:771781. 1989

    54. Antonio, J., and W.J. Gonyea. Skeletal muscle fiber hyperplasia. Med. Sci.

    Sports Exerc.25:13331345. 1993.

    55. Antonio, J., and W.J. Gonyea. Muscle fiber splitting in stretch-enlarged avian

    muscle. Med. Sci. Sports Exerc.26:973977. 1994..

    56. Gardiner, P.F., B.J. Jasmin, and P. Corriveau. Rostrocaudal pattern of fiber-type

    changes in an overloaded rat ankle extensor.J. Appl. Physiol.71:558564. 1991.

    57. Brown, J.M.M., C. Solomon, and M. Paton. Further evidence of functionaldifferentiation within biceps brachii. Electromyogr. Clin. Neurophysiol.33:301309.

    1993

    58. English, A.W., S.L. Wolf, and R.L. Segal. Compartmentalization of muscles andtheir motor nuclei: The partitioning hypothesis. Phys. Ther.73:857867. 1993.

    59. Wickiewicz, T.L., R.R. Roy, P.L. Powell, and V.R. Edgerton. Muscle architectureof the human lower limb. Clin. Orthop. Related Res.179:275283. 1983

    60. Heron, M.I., and F.J.R. Richmond. In-series fiber architecture in long humanmuscles.J. Morphol.216:3545. 1993.

    61. Lindman, R., A. Eriksson, and L.-E. Thornell. Fiber type composition of the

    human male trapezius muscle: Enzymehistochemical characteristics.Am. J. Anat.189:236244. 1990

    62. Lindman, R., A. Eriksson, and L.-E. Thornell. Fiber type composition of the

    human female trapezius muscle: Enzymehistochemical characteristics.Am. J. Anat.190:385392. 1991.

    63. Haussinger D. Control of protein turnover by the cellular hydratation state. Ital

    J Gastroenterol. 1993 Jan;25(1):42-8.

    64. Tesch, P.A., and L. Larsons. Muscle hypertrophy in bodybuilders. Eur. J. Appl.

    Physiol. 49:301306. 1982

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