Each muscle fiber is a single, multinucleated
cell, made up of smaller units called myofibrils. Myofibrils have
a repeating pattern called a sarcomere, which is the basic functional
unit of muscles. The myofibril is made up of even smaller structures called
myofilaments, which are long chains of proteins actin and myosin.
Another set of proteins regulates the
interaction between actin and myosin. In the actin thin filament there’s a
binding site that a myosin head can reach and grab, but the binding sites are
covered. Calcium causes configurational changes and uncovers the binding sites
for myosin. This calcium is stored in muscle cells in the sarcoplasmic
reticulum distributed around the myofibrils.
Strength training can result in localized muscle
tissue damage. When a certain threshold is exceeded, sarcomeres break.
(It is assumed that optimum sarcomere length is 2.5 μm). This damages contractile
elements or myofibrillar structures, disrupts the sarcolemma and sarcoplasmic
reticular, causes damage to supportive connective tissue and injuries in the
cytoskeleton (1).
This damage generate a hypertrophic response (2,
3). Muscle damage is a frequent response after unaccustomed exercise, or when
performing high intensity exercise. A trainee may experience stiffness and delayed-onset
muscle soreness. Other metabolic consequences are increases in
creatine-kinase, muscle troponin I, myoglobin and heavy myosin chain (4).
Eccentric actions
The best way to induce micro tears is by
emphasizing eccentric training. The eccentric contraction has been
proven through countless studies to cause the most damage, which has
been shown to mediate a hypertrophic response (5,6), causing myofibrillar
remodeling (7,8).
The distribution of sarcomeres on each myofibril
is nonuniform, the weakest sarcomeres are located at different regions. This nonuniform
lengthening causes a shearing of myofibrils and deforms membranes (4).
The presence of disrupted sarcomeres in
myofibrils and damage to the excitation–contraction (E–C) coupling
system are signs of damage in a muscle from eccentric exercise (9).
During active stretch of a muscle, most of the
length change will be taken up by the weakest sarcomeres (10) in myofibrils
(the weakest half-sarcomeres). These sarcomeres become progressively weaker and
then lengthen rapidly, uncontrollably, to a point of no myofilament overlap.
Then overstretched sarcomeres are distributed at random along muscle fibers.
When the muscle relaxes, some myofilaments in the majority of overstretched
sarcomeres become disrupted (11).
During repeated eccentric contractions it is
postulated that the number of disrupted sarcomeres grows, until a point is
reached where membrane damage occurs. It is at this point that damage to
elements of the E–C coupling machinery becomes apparent. Subsequently the fiber may die (12) (Fig. 1).
Membrane damage begins with tearing of t-tubules
followed by damage to the sarcoplasmic reticulum, uncontrolled Ca2+ release. If
the damage is extensive enough, parts of the fiber, or the whole fiber may
die. Breakdown products of dead and dying cells would lead to a local
inflammatory response associated with tissue oedema and soreness (12). Although
it’s not clear, the first step in the damage process can be t-tubule rupture,
leading to inactivation of some sarcomeres, but the reverse sequence beginning
with sarcomere disruptions can also lead to t-tubule damage (12).
There are also observations of abnormal
t-tubular arrangements after eccentric exercise (13).
Eccentric actions and force generation
Muscles achieve higher absolute forces when
contracting eccentrically (14,15,16). Heavy negatives, or supramaximal
eccentric actions involve eccentric contractions at a weight greater than
concentric 1RM. It has been shown that eccentric strength is
approximately 20–50% greater than the concentric strength (17) and even
predicted to be up to 64% greater (52).
Eccentric contractions could stimulate greater
adaptations (18), because increases in strength are thought to be
proportional to the magnitude of force developed (19).
Eccentric training is more effective at
increasing total and eccentric strength than concentric training, and
appears to be more effective at increasing muscle mass than concentric
training, possibly because of the higher forces developed. Adaptations after
eccentric training are highly specific to the velocity and type of contraction
(20).
Eccentric exercise preferentially recruit
fast twitch muscle fibers (53,21,22,23) and perhaps recruitment of
previously inactive MUs (21,24). This results in an increased mechanical
tension in type II fibers, which have the greatest potential for muscle
growth (53,25,26,27).
Compared with concentric contractions,
eccentric contractions also produce less fatigue and are more
efficient at metabolic level. Unaccustomed eccentric contractions produce
transient muscle damage, soreness and force impairments.
Eccentric actions and protein synthesis
Passive muscular tension develops because of
lengthening of extra myofibrillar elements, especially collagen (28). This
increases the active tension enhancing the hypertrophic response.
Eccentric contractions elicits greater gains
in lean muscle compared with concentric and isometric contractions
(29,30,31,32). Maximal muscle hypertrophy can only be attained if eccentric
muscle actions are performed (33).
When lifting the same weight concentrically and
eccentrically no significant difference between the two contractions is
observed, if volume is equalized. However in a few studies there’s was a slight
advantage for the excentric actions (34,54). Excentric actions are best done
supramaximal, above 1RM concentric load.
Lengthening the muscle increase protein
synthesis more than a concentric contraction (34), in part by releasing phosphatidic
acid, which encourages protein synthesis (35). Another pathway is through
the activation of satellite cells located on the outside of muscles.
Satellite cells move to the damaged area and fuse to muscle, becoming a part of
it (36), increasing muscle fiber size by the addition of the satellite cell's
nucleus to the muscle.
The more nuclei, the greater the growth
potential. Plateau happens when we can't adequately activate satellite cells
(37,38), therefore maximize eccentric loading may be very beneficial.
Other increases have also been observed, such as
a faster rise in protein synthesis (39), greater increases in IGF-1
messenger RNA (mRNA) expression (40), and more pronounced elevations in p70S6k
(41), when compared with other types of contractions.
As for the tempo, faster speed eccentric
contractions release more growth factors, more satellite cells, and
greater protein synthesis than slow speed eccentric contractions (42,43). A
2- to 3-second tempo is hypothesized to be ideal for maximizing a hypertrophic
response (43).
Eccentric training is also associated with an increased
metabolic stress. Higher eccentric intensities elevate lactate buildup and
spike anabolic hormonal levels (44).
However another important note: acute measures
(1-6h post exercise) of MPS following an initial exposure to RE in novices are
not correlated with muscle hypertrophy following chronic RT (55). There’ also a
review on the relationship between acute of muscle protein synthesis response
and changes in muscle mass (56). Muscle protein breakdown is also important for
the regulation of muscle hypertrophy on the long term, and the chronic
(positive) balance between MPS and MPB is more important.
Muscle swelling and soreness
In human subjects, the initial fall in tension
after eccentric exercise is followed by a slow rise over 2–4 h, presumably
recovery from metabolic exhaustion. Then 24 h later there’s a second fall in
tension (45).
Eccentric exercise is followed by sensations of
stiffness and soreness the next day (46), transient muscle damage, soreness and
force impairments (47).
Because of eccentric exercise the contracting
muscle is forcibly lengthened. Delayed muscle soreness sets in at about 6–8h
after the exercise and peaks at about 48 h (45,48). A second bout of eccentric
exercise, a week after the first, leaves us much less stiff and sore.
The injury triggers a local inflammatory
response that is accompanied by some oedema. The breakdown products of
injured tissues sensitize nociceptors (12,45,49). These nociceptors
respond to stimuli that are normally non-noxious, leaving the muscle tender to
local palpation, stretch and contraction. A component of the delayed soreness
from eccentric exercise may involves large-fiber mechanoreceptors (50,51).
The repair mechanism involves the addition of
sarcomeres to regenerating muscle fiber, as shown by animal experiments.
Neutrophils migrate to the area of micro trauma. Damaged
fibers release several agents that attract macrophages and lymphocytes
to the injury site. The purpose of macrophages is to remove cellular debris and
to produce cytokines that activate myoblasts, macrophages and
lymphocytes. This response triggers the release of various growth factors
that regulate satellite cell proliferation and differentiation (44).
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References:
1. Hill, M and Goldspink, G. Expression and
splicing of the insulin-like growth factor gene in rodent muscle is associated
with muscle satellite (stem) cell activation following local tissue damage. J
Physiol 549: 409–418, 2003.
2. Izquierdo, M, Ibanez, J, Gonzalez-Badillo,
JJ,Hakkinen, K, Ratamess, NA, Kraemer, WJ, French, DN, Eslava, J, Altadill,
A,Asiain, X, and Gorostiaga, EM. Differential effects of strength training
leading to failure versus not to failure on hormonal responses, strength and
muscle power increases. J Appl Physiol 100: 1647–1656, 2006.
3. Evans, WJ. Effects of exercise on senescent
muscle. Clin Orthopaed Rel Res 403(Suppl.): S211–S220, 2002.
4. Tee JC, Bosch AN, Lambert MI (2007).
Metabolic consequences of exercise induced muscle damage. Sports Med 37:
827-836.
5. Evans WJ. Effects of exercise on senescent
muscle. Clin Orthop Relat Res 403(Suppl): S211–S220, 2002.
6. Hill M and Goldspink G. Expression and
splicing of the insulin-like growth factor gene in rodent muscle is associated
with muscle satellite (stem) cell activation following local tissue damage. J
Physiol 549:409–418, 2003.
7. Crameri RM, Langberg H, Magnusson P, Jensen
CH,Schroder HD, Olesen JL, and Kjaer M. Changes in satellite cells in human
skeletal muscle after a single bout of high intensity exercise. J Physiol
558:333–340, 2004.
8. Yu JG and Thornell LE. Desmin and actin
alterations in human muscles affected by delayed onset muscle soreness: A high
resolution immunocy to chemical study. Histochem Cell Biol 118: 171–179, 2002.
9. Warren,G. L. Ingalls, C.P. Lowe, D.A.
Armstrong, R.B. (2001). Excitation-contraction uncoupling: major role in
contraction-induced muscle injury. Exercise and Sport Sciences Reviews 29,
82–87.
10. Morgan, D. L. (1990). New insights into the
behavior of muscle during active lengthening. Biophysics Journal 57,209–221.
11. Talbot, J. A. & Morgan, D. L. (1996).
Quantitative analysis of sarcomere non-uniformities in active muscle following
a stretch. Journal of Muscle Research and Cell Motility 17,261–268.
12. U. Proske D. L. Morgan. Muscle damage from
eccentric exercise: mechanism, mechanical signs,adaptation and clinical
applications. Journal of Physiology (2001),537.2, pp.333–345
13. Takekura H., Fujinami, N., Nishizawa, T.,
Ogasawara,H. & Kasuga, N. (2001). Eccentric exercise-induced morphological
changes in the membrane systems involved in excitation– contraction coupling in
rat skeletal muscle. Journal of Physiology 533, 571–583.
14. Crenshaw AG, Karlsson S, Styf J, et al. Knee
extension torque and intramuscular pressure of the vastus lateralis muscle
during eccentric and concentric activities. Eur J Appl Physiol 1995;70:13–19.
15. Westing SH, Cresswell AG, Thortensson A.
Muscle activation during maximal voluntary exercise and concentric knee
extension. EurJ Appl Physiol 1991;62:104–8.
16. Westing SH, Seger JY. Eccentric and
concentric torque velocity characteristics, torque output comparisons and
gravity effect torque corrections for the quadriceps and hamstring muscles in
females. Int J Sports Med 1989;10:175–80
17. Bamman MM, Shipp JR, Jiang J, Gower BA,
Hunter GR,Goodman A, McLafferty CL, and Urban RJ. Mechanical load increases
muscle IGF-1and androgen receptor mRNA concentrations in humans. Am J Physiol
Endocrinol Metab 280: E383–E390, 2001
18. Hather BM, Tesch PA, Buchanan P, et al.
Influence of eccentric actions on skeletal muscle adaptations to resistance
training. Acta Physiol Scand 1991;143:177–85
19. Goldberg AL, Etlinger JD, Goldspink DF, et
al. Mechanism of work-induced hypertrophy of skeletal muscle. Med Sci Sports
Exerc1975;7:185–98.
20. M Roig, K. O’Brien, G. Kirk, R. Murray,
P.McKinnon, B. Shadgan,W. D. Reid. The effects of eccentric versus concentric
resistance training on muscle strength and mass in healthy adults: a systematic
review with meta-analysis, Br J Sports Med 2009; 43:556–568.
21. Nardone A, Romano, C, and Schieppati M.
Selective recruitment of high-threshold human motor units during voluntary
isotonic lengthening of active muscles. J Physiol 409: 451–471, 1989.
22. Shepstone TN, Tang JE, Dallaire S, Schuenke
MD,Staron RS, and Phillips SM. Short-term high- vs. low-velocity isokinetic
lengthening training results in greater hypertrophy of the elbow flexors in young
men. J Appl Physiol 98: 1768–1776, 2005.
23. Takarada Y, Takazawa H, Sato Y, Takebayashi
S, Tanaka Y, and Ishii N. Effects of resistance exercise combined with moderate
vascular occlusion on muscular function in humans. J Appl Physiol 88:2097–2106,
2000.
24. McHugh MP, Connolly DA, Eston RG, and Gleim
GW. Electromyographic analysis of exercise resulting in symptoms of muscle
damage. J Sport Sci 18: 163–172, 2000.
25. Hortoba´ gyi, T, Barrier J, Beard D,
Braspennincx J, and Koens J. Greater initial adaptations to submaximal muscle
lengthening than maximal shortening. J Appl Physiol 81: 1677–1682, 1996
26. Kosek DJ, Kim JS, Petrella JK, Cross JM, and
Bamman MM. Efficacy of 3 days/wk resistance training on myofiber hypertrophy
and myogenic mechanisms in young vs. older adults. J Appl Physiol 101:
531–544,2006.
27. Tesch PA. Skeletal muscle adaptations
consequent to long-term heavy resistance exercise. Med Sci Sports Exerc 20(5
Suppl):S132–S134, 1988.
28. Toigo, M and Boutellier, U. New fundamental
resistance exercise determinants of molecular and cellular muscle adaptations.
Eur J Appl Physiol 97: 643–663, 2006.
29. Farthing JP and Chilibeck PD. The effects of
eccentric and concentric training at different velocities on muscle
hypertrophy. Eur J Appl Physiol 89: 578–586, 2003.
30. Friedmann B, Kinscherf R, Vorwald S, Muller,
H,Kucera K, Borisch S, Richter G, Ba¨ rtsch P, and Billeter R. Muscular
adaptations to computer-guided strength training with eccentric overload. Acta
Physiol Scand 182: 77–88, 2004.
31. Higbie EJ, Cureton KJ, Warren GL III, and
Prior BM. Effects of concentric and eccentric training on muscle strength,
cross-sectional area, and neural activation. J Appl Physiol 81: 2173–2181,
1996.
32. Norrbrand L, Fluckey JD, Pozzo M, and Tesch
PA.Resistance training using eccentric overload induces early adaptations
inskeletal muscle size. Eur J Appl Physiol 102: 271–281, 1989.
33. Hather BM, Tesch PA, Buchanan P, and Dudley
GA. Influence of eccentric actions on skeletal-muscle adaptations to resistance
training. Acta Physiol Scand 143: 177–185, 1991.
34. Eliasson J, et al. Maximal lengthening
contractions increase p70 S6 kinase phosphorylation in human skeletal muscle in
the absence of nutritional supply. Am J Physiol Endocrinol Metab. 2006
Dec;291(6):E1197-205.
35. O'Neil TK, et al. The role of
phosphoinositide 3-kinase and phosphatidic acid in the regulation of mammalian
target of rapamycin following eccentric contractions. J Physiol. 2009 Jul
15;587 (Pt 14):3691-701.
36. Rosenblatt JD, et al. Satellite cell
activity is required for hypertrophy of overloaded adult rat muscle. Muscle
Nerve. 1994Jun;17(6):608-13.
37. Bamman MM, et al. Cluster analysis tests the
importance of myogenic gene expression during myofiber hypertrophy in humans. J
Appl Physiol (1985).2007 Jun;102(6):2232-9.
38. Petrella JK, et al. Potent myofiber
hypertrophy during resistance training in humans is associated with satellite
cell-mediated myonuclear addition: a cluster analysis. J Appl Physiol (1985).
2008 Jun;104(6):1736-42.
39. Moore DR, Phillips SM, Babraj JA, Smith K,
and Rennie MJ. Myofibrillar and collagen protein synthesis in human skeletal
muscle in young men after maximal shortening and lengthening contractions. Am J
Physiol Endocrinol Metabol 288: E1153–E1159, 2005.
40. Shepstone TN, Tang JE, Dallaire S, Schuenke
MD,Staron RS, and Phillips SM. Short-term high- vs. low-velocity isokinetic
lengthening training results in greater hypertrophy of the elbow flexors
inyoung men. J Appl Physiol 98: 1768–1776, 2005.
41. Eliasson J, Elfegoun T, Nilsson J, Kohnke
R,Ekblom B, and Blomstrand E. Maximal lengthening contractions increase p70
S6kinase phosphorylation in human skeletal muscle in the absence of
nutritionalsupply. Am J Physiol Endocrinol Metabol 291:E1197–E1205, 2006.
42. Moore DR, et al. Myofibrillar and collagen
protein synthesis in human skeletal muscle in young men after maximal
shortening and lengthening contractions. Am J Physiol Endocrinol Metab. 2005
Jun; 288(6):E1153-9.
43. Shepstone TN, et al. Short-term high- vs.
low-velocity isokinetic lengthening training results in greater hypertrophy of
the elbow flexors in young men. J Appl Physiol (1985). 2005 May; 98(5):1768-76.
44. Schoenfeld BJ. The mechanisms of muscle
hypertrophy and their application to resistance training. J Strength Cond
Res24: 2857–2875, 2010.
45. Macintyre, D. L., Reid, W. D. &
Mckenzie, D.C. (1995). Delayed muscle soreness. The inflammatory response to
muscle injury and its clinical implications. Journal of Sports Medicine 20,24–40.
46. Hough, T. (1902). Ergographic studies in
muscular soreness. American Journal of Physiology 7, 76–92.
47. Byrne C, Twist C, Eston R. Neuromuscular
function after exercise-induced muscle damage. Sports Med 2004;34:49–69.
48. Jones, C., Allen, T., Talbot, J., Morgan, D.
L.& Proske, U. (1997). Changes in the mechanical properties of human and
amphibian muscle after eccentric exercise. European Journal of Applied
Physiology and Occupational Physiology 76, 21–31.
49. Smith, L. L. (1991). Acute inflammation: the
underlying mechanism in delayed onset muscle soreness? Medicine and Science
inSports and Exercise 23, 542–551.
50. Barlas, P., Walsh, D. M., Baxter, G. D.
& Allen,J. M. (2000). Delayed onset muscle soreness: effect of an ischaemic
block upon mechanical allodynia in humans. Pain 87, 221–225.
51. Weerakkody, N. S. Whitehead, N.P. Canny, B.
J.Gregory J. E. & Proske. (2001). Large-fiber mechano receptors contribute
to muscle soreness after eccentric exercise. Journal of Pain 2,209–219.
52. Moir GL, Erny KF, Davis SE, Guers JJ, Witmer
CA.The Development of a Repetition-Load Scheme for the Eccentric-Only Bench
Press Exercise. J Hum Kinet. 2013 Oct 8;38:23-31.
53. Brad Schoenfeld. The Use of Specialized
Training Techniques to Maximize Muscle Hypertrophy. Strength & Conditioning
Journal: August 2011 - Volume 33 - Issue 4 - pp 60-65
54. Mayhew TP, et al. Muscular adaptation to
concentric and eccentric exercise at equal power levels. Med Sci Sports
Exerc.1995 Jun;27(6):868-73.
55. Mitchell CJ, Churchward-Venne TA, Parise G,
Bellamy L, Baker SK, et al. (2014) Acute Post-Exercise Myofibrillar Protein
Synthesis Is Not Correlated With Resistance Training-Induced Muscle Hypertrophy
in Young Men. PLoS ONE 9(2): e89431.
56. Cameron J. Mitchell , Tyler A.
Churchward-Venne , David Cameron-Smith , Stuart M. Phillips. What is the
relationship between the acute muscle protein synthetic response and changes in
muscle mass? Journal of Applied PhysiologyPublished 25 September
2014
