Hypertrophy - Muscular Growth
Hypertrophy 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 a myofibril. These allow for the expression of musculature contraction.
Adaptations within these structures are a consequence of contractile demands on
the system itself. The increase seen can be viewed grossly through two
mechanisms. The first adaptation concerns the addition of myofilaments to the
peripheral or outer region of the 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 is made 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
synthesis for 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 in regards to contractile tissue is literally
heightened, resulting in a super compensation effect (an effect which raises
structural and contractile tissue to above pre training bout 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 acid group,
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 in order to augment the supercompensatory process previously
described.
Why Moderate Reps Stimulate Optimal Hypertrophy
Evidence suggests that moderate repetition sets provide an optimal stimulus
for growth in the fast twitch fibers, while high repetition sets may optimize
the hypertrophy process in slower twitch fibers. Reasons follow. First, sets
which fall within 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 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 into play (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
adaptations to imposed demands. Interestingly enough, much evidence supports the
postulate that 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 of work.
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 any
enzyme 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 lactate concentration 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 a result of a direct stimulatory
effect of lactate on the secretion of testosterone by increasing testicular cAMP
production. Consequently blood lactate levels rise highest in 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 athlete’s one repetition maximum. 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 carry blood 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 build up 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 of protein 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 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 will lead 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 specific fiber 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 undermine the participants training efficiency. Further,
if a muscle is predominantly slow twitch and 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 slow twitch. 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 recommendation would 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 be delineated 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 fast twitch 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 repetition set at the end of the workout.
Note: Muscle Fiber Ratios are provided in the Anatomy Section of the Site
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!
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 your others normally.
Jacob Wilson
Trainer@abcbodybuilding.com
President Abcbodybuilding
References and Sources Cited
1. Zehr, E.P. Ballistic movement: Muscle activation and neuromuscular
adaptation. Can. J. Appl. Physiol. 19:(4)363–378. 1994.
3. Schoenfeld, Brad, 2000: Repetitions and Muscle Hypertrophy.
Strength and Conditioning Journal: Vol. 22, No. 6, pp. 67–69.
4. 8. Kraemer, W.J. Changes in hormonal concentrations after different
heavy-resistance exercise protocols in women. J. Appl. Physiol.
75:(2)594–604. 1993.
5. Lu, S.S. Lactate and the effects of exercise on testosterone secretion:
Evidence for the involvement of a cAMP-mediated mechanism. Med. Sci. Sports
Exerc. 29:(8)1048–1054. 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
exercise protocols. J. Appl. Physiol. 69:(4)1442–1450. 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)228–235. 1991.
9. Wilmore, J.H. Physiology of Sport and Exercise. (2nd ed.). Champaign,
IL: Human Kinetics, 1999.
10. 4. Häussinger, D. Cellular hydration state: An important determinant of
protein catabolism in health and disease. Lancet. 341:(8856)1330–1332.
1993.
11. Millar, I.D. Mammary protein synthesis is acutely regulated by the
cellular hydration state. Biochem. Biophys. Res. Commun. 230:(2)351–355.
1997.
12. Waldegger, S. Effect of cellular hydration on protein metabolism.
Miner. Electrolyte Metab. 23:(3–6)201–205. 1997
13. Evans, W.J. The metabolic effects of exercise-induced muscle damage.
Exerc. Sport Sci. Rev. 19: (-HD-). 99–125. 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.
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.
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. 9:222–227. 1995.
32. Brown, J.M.M., C. Solomon, and M. Paton.
Further evidence of functional differentiation within biceps brachii.
Electromyogr. Clin. Neurophysiol. 33:301–309. 1993.
33. 29. Glass, S.C., and T. Armstrong.
Electromyographical activity of the pectoralis muscle during decline bench
presses. J. Strength Cond. Res. 11:163–167. 1997.
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. 77:1293–1297. 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 changes in muscle architecture and specific tension. Eur. J.
Appl. Physiol. 72:37-43 1995.
39. ANTONIO, JOSE, 2000: Nonuniform Response of Skeletal Muscle to Heavy
Resistance Training: Can Bodybuilders Induce Regional Muscle Hypertrophy?.
The Journal of Strength and Conditioning Research: Vol. 14, No. 1, pp.
102–113.
40. Elder, G.C.B., K. Bradbury, and R. Roberts. Variability of fiber type
distributions within human muscles. J. Appl. Physiol. 53:1473–1480. 1982.
41. Punkt, K., H. Mehlhorn, and H. Hilbig. Region- and age-dependent
variations of muscle fiber properties. Acta Histochem. 100:37–58. 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:S315–S319. 1992.
44.
Johnson, M.A., Polgar, J., Weightman, D. &
Appleton, D. (1973). Data on the distribution 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
stretch overloaded quail muscle. Acta Physiol. Scand. 152:429–430. 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. 151:135–142. 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. 140:175–180. 1990.
50. Sakuma, K., A. Yamaguchi, and S. Katsuta. Are region-specific changes in
fibre types attributable to nonuniform muscle hypertrophy by overloading?.
Eur. J. Appl. Physiol. 71:499–504. 1995.
51. Alway, S.E. Stretch induces non-uniform isomyosin expression in the
quail anterior latissimus dorsi muscle. Anat. Rec. 237:1–7. 1993
52. Alway, S.E., W.H. Grumbt, J. Stray-Gundersen, and W.J. Gonyea. Effects
of resistance training on elbow flexors of highly competitive bodybuilders.
J. Appl. Physiol. 72:1512–1521. 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. 66:771–781. 1989
54. Antonio, J., and W.J. Gonyea. Skeletal muscle fiber hyperplasia.
Med. Sci. Sports Exerc. 25:1333–1345. 1993.
55. Antonio, J., and W.J. Gonyea. Muscle fiber splitting in stretch-enlarged
avian muscle. Med. Sci. Sports Exerc. 26:973–977. 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.
71:558–564. 1991.
57. Brown, J.M.M., C. Solomon, and M. Paton. Further evidence of functional
differentiation within biceps brachii. Electromyogr. Clin. Neurophysiol.
33:301–309. 1993
58. English, A.W., S.L. Wolf, and R.L. Segal. Compartmentalization of
muscles and their motor nuclei: The partitioning hypothesis. Phys. Ther.
73:857–867. 1993.
59. Wickiewicz, T.L., R.R. Roy, P.L. Powell, and V.R. Edgerton. Muscle
architecture of the human lower limb. Clin. Orthop. Related Res.
179:275–283. 1983
60. Heron, M.I., and F.J.R. Richmond. In-series fiber architecture in long
human muscles. J. Morphol. 216:35–45. 1993.
61. Lindman, R., A. Eriksson, and L.-E. Thornell. Fiber type composition of
the human male trapezius muscle: Enzyme–histochemical characteristics. Am. J.
Anat. 189:236–244. 1990
62. Lindman, R., A. Eriksson, and L.-E. Thornell. Fiber type composition of
the human female trapezius muscle: Enzyme–histochemical characteristics. Am.
J. Anat. 190:385–392. 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. 49:301–306. 1982
