acta academiae olympiquae estoNiae

Transcription

acta academiae olympiquae estoNiae
National olympic committee of Estonia
ACTA academiae
olympiquae Estoniae
Indexed in International Databases of Sportdata
and EBSCO Publishing SPORTDiscus with Fulltext
VOL. 14 Number 1/2 , 2006 TARTU
Editor in Chief
ARVED VAIN Dr. Habil. Biol.
Faculty of Physics and Chemistry, University of Tartu, Tartu
Tähe 4-203
51010 Tartu
Estonia
Editorial Board
VAHUR ÖÖPIK PhD
Faculty of Exercise and Sport Sciences, University of Tartu, Tartu
MEHIS VIRU PhD
Faculty of Exercise and Sport Sciences, University of Tartu, Tartu
REELE REMMELKOOR
Faculty of Medicine, University of Tartu, Tartu
GUNNAR PAAL PhD
The Riigikogu (the Estonian Parliament), Tallinn
ULRICH HARTMANN PhD
Technical University of Munich, Munich
Proofreader
MARE VENE, Tartu
Contents
Olympism practique.
Preparation for olympic games
Karin Alev, Teet Seene –
Effect of endurance training on the character of skeletal
muscle kinetics
5
Toomas Karu, Ants Nurmekivi, Jaan Loko, Tõnis Saag –
Is strength training in sport centre an aerobic activity?
18
Jaan Ereline, Helena Gapeyeva, Mati Pääsuke –
Twitch contractile properties of plantarflexor muscles in Nordic
combined athletes and cross-country skiers
25
Arved Vain –
The phenomenon of mechanical stress transmission in
skeletal muscles
38
M. Vahimets, H. Gapeyeva, J. Ereline, M. Pääsuke, P. Kaasik,
A. Vain – Influence of trigenics myoneural treatment on lower
extremities’ muscle tone and viscous-elastic properties in young
basketball players
49
AS Atlex
Kivi 23
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Phone +372 734 9099
Fax +372 734 8915
e-mail: atlex@atlex.ee
CHRONICLES OF THE ESTONIAN
OLYMPIC ACADEMY
Darja Saar –
46th International Session for young participants
70
ISSN 1406-1287
Information for Contributors
78
Acta Academiae Olympiquae Estoniae Vol. 14 No. 1/2, pp 5–17, 2006
EFFECT OF ENDURANCE TRAINING ON THE
CHARACTER OF SKELETAL MUSCLE KINETICS
Karin Alev, Teet Seene
Institute of Exercise Biology and Physiotherapy, University of Tartu
Role of oxidative capacity of muscle fibres in endurance training
Olympism practique.
Preparation for olympic games
Endurance training promotes numerous adaptations in skeletal muscle,
including enhancement of fibre oxidative capacity and muscle phenotype
transitions. It has been demonstrated that aerobic endurance training leads
to metabolic [36] and structural changes not only in slow-twitch (ST) but
also in fast-twitch (FT) muscle fibres [15, 31]. Changes in the expression
of myosin heavy chain (MyHC) and myosin light chain (MyLC) isoforms
are in good agreement with the above-mentioned findings [28]. Endurance
training increased the oxidative capacity in the plantaris muscle by 16%
and in the extensor digitorum longus muscle by 12%. It has been shown
that exercise training in FT fibres causes up-regulation of MyHC IIa and IIx
isoforms, whereas the MyHC IIb is down-regulated [10]. Multidirectional
changes have also been revealed in the relative contents of MyHC isoforms
in different FT muscles if the training volume is increased [29]. These changes might be related to the differences in oxidative capacity of muscles [31].
Until now the question to what extent gene expression of MyHC isoforms
is due to genetic predisposition or to the specificity of training remains
unanswered [1].
Changes in molecular motor of contractile machinery in
endurance training
The contractile protein myosin plays an important role in dictating the functional properties of skeletal muscle fibres. Myosin is known to exist as multiple isoforms in skeletal muscle as a result of polymorphic expression of
both heavy and light chain components. It is unlikely that the whole variability in contractile machinery during endurance training depends on the
content of MyHC isoforms. MyHC isoforms are the main determinants of
muscle contraction, but it has been shown there is also some ground to believe that MyLC has a functional significance in the process of adaptation of
sarcomeric proteins to the long-lasting exercise.
As a myosin molecule is formed by MyHC and MyLC isoforms and the
functional significance of both in muscle contraction has been proved, it
should be more useful to study the expression of MyHC and MyLC isoforms
in parallel during endurance exercise training in order to obtain information
about the adaptive pecularities in the contractile machinery.
The effect of endurance exercise on the MyHC profile appears to be both
muscle specific and dose dependent, increase in the duration of training resulted in a progressive fast-to-slow shift in MyHC composition in rat skeletal muscle [10]. Wahrmann et al. [41] reported obvious fast-to-slow transitions of MyHC and MyLC profiles in rat hindlimb muscles with controlled
regimens of endurance training. Edurance training also evokes transition in
MyHC isoforms, in most cases transitions are limited to the fast-type subtypes and thus consist of a decrease of the fastest MyHC IIb isoform with
attendedant increase in the MyHC IIa isoform [37].
The decrease of MyHC IIb isoforms during endurance training in FT
muscles does not necessarily show that in these muscles contractile properties change towards ST as the relative content of MyHC IIa and IId isoforms
increases [28]. Rather, these changes show that it is more economical for the
FT muscles to perform the exercise. The decrease in slow isoforms both in
alkali and regulatory MyLC during endurance training and the increase in
MyLC 3f isoforms in FT muscles is at first glance not in logical agreement
with changes in the MyHC isoform pattern. However, the stoichiometry of
these subunits and their association with each other do not change (MyHC
IIb decreased but IId increased and MyLC 3f is associated with both, IIb and
IId MyHC to form myosin molecules). This shows that there are no definite
adaptational borders between MyHC and MyLC isoforms in FT muscles to
the long-lasting endurance exercise [28]. The adaptation process consists of
both changes in MyHC and MyLC during aerobic endurance training and
MyLC may also be associated with transformation of muscle function [29].
The slowest and fastest MyHC isoforms have a higher sensitivity to the
process of degradation. In myopathic FT muscles MyHC IIb isoform is more
sensitive to the serine proteinase than other isoforms [30]. Together with the
slower synthesis rate [29] this may also explain the decrease in the MyHC
IIb isoform in FT muscles during six weeks of endurance exercise.
Changes in contractile proteins turnover rate in
endurance training
As all myofibrillar proteins are in the continuous process of synthesis and
degradation, changes in the turnover rate of the main contractile protein,
myosin molecule, characterize these renewal processes in the contractile
apparatus during the adaptation to the aerobic endurance training. The turn­
over of MyHC and MyLC isoforms provides a mechanism by which the
type and amount of protein can be changed in accordance with the needs
of contractile machinery during the adaptation to the exercise training [29].
It has been demonstrated that the turnover rate of MyHC isoforms shows
differences between the FT muscles. The turnover rate is faster in FT muscles with a higher oxidative potential. Myosin turnover supports qualitative
remodelling of FT muscles, so that the former pattern of MyHC and MyLC
isoforms is changing, and the contractile process is better suited to new conditions of long-lasting muscle activity [1].
Changes in the turnover rate of MyHC isoforms in the FT muscles during the adaptation to the endurance training characterize also changes in the
myofibrillar apparatus through protein metabolism [28, 29]. The latitude of
changes (increase, decrease) in the turnover rate of a certain myosin isoform
shows also the significance of MyHC isoforms in the process of adaptation
to the endurance training. During endurance training MyHC IIa, IIb, IId, and
MyLC 2s and 3f isoforms in FT muscles reflected explicitly the process of
adaptation through changes in the relative content of myosin isoforms.
When seeking an answer to the question how does the prolonged mechanical activity affect the contractile apparatus in FT muscles, it is expedient
to begin with the backbone – the myosin molecule. Although the exact role
of MyLC isoforms in FT muscles during the adaptation to the aerobic endurance training is not fully known, changes in the relative content of MyLC
isoforms and their relations with the character of training show that they
play an important role in the process of modulation of contractile machinery
during the increase in the oxidative capacity and more intensive degradation
rate of contractile proteins [29, 32]. Simultaneously with increased degradation of contractile proteins, endurance training also increased the degradation rate of MyHC isoforms. The degradation rate of MyHC isoforms
increases in spite of the increase in the oxidative potential of the FT skeletal
muscle. The decrease in the expression of MyHC IIb isoform in FT muscles is caused by the intensive degradation of the isoform during endurance
training, which is probably the main reason for unchanged turnover rate of
MyHC IIb isoform in endurance-trained rats [28]. During the adaptation
to the long-lasting endurance exercise a decrease in MyHC IIb isoform in
FT skeletal muscle points to the transformation of the muscle contractile
apparatus in accordance with the increase in muscle oxidative capacity. This
adaptational process shows coordination between changes in oxidative capacity and contractile machinery in skeletal muscle during the adaptation
to the endurance training first of all in relation to muscle metabolism [29].
Adaptational processes in FT muscles during endurance training show high
potential of recruiting these muscles [28].
Role of myosin in the diversity of skeletal muscle fibres
The generation of muscle fibre heterogenity is based on the gene regulation
through two main mechanisms.
1. Qualitative mechanism – muscle protein (like myosin) may exist in forms,
which are similar but not identical (isoforms). Replacement of isoforms
represents the frist mechanism generating diversity among muscle fibres
2. Quantitative mechanism – differential expression of the same gene. The
proportion of the products of these genes will therefore be modified and
new functional or structural features will appear [7].
During muscle development from embryonic till adult stage several myosin
isoforms are sequentially expressed. Synthesis of these isoforms is repressed at a given stage of development when they are replaced by the adult
isoforms [42].
Myosin plays an important role in dictating the functional properties
of skeletal muscle fibres. Myosin is known to exist as multiple isoforms
in striated muscle as a result of polymorphic expression of both its heavy
and light chain components [12]. At present nine distinct isoforms of the
MyHC have been identified in mammalian skeletal muscle, of which four
are thought to be expressed in rodent limb muscles [25]. Like the other
contractile proteins the MyLC represents a family of isoforms, at least three
isoforms of the alkali LC (one slow − LC1s and two fast − LC1f and LC3f)
and two isoforms of the regulatory LC − LC2s and LC2f have been identified
in rat skeletal muscle.
Changes in the expression of MyLC can be included in FT muscle by
chronic low-frequency stimulation [9]. Stimulation induces a sequential
exchange of fast light-chain isoforms with their slow counterparts. In vitro
experiments show, the alterations at the translation process change the pattern of specific mRNAs. Studies of co-existence of MyHC and MyLC isoforms in the same muscle fibre show that MyHC IIa is preferably associated
with MyLC 1f, whereas MyHC IIb is favourably associated with MyLC 3f.
Early studies of Pette et al. [24] considered that variations in an amount of
MyLC 3f in single type II fibres reflected subpopulations of type II fibres.
Prolonged endurance training elicits a decrease in the ratio of MyLC 3f
to MyLC 1f concurrently with the transformation from type MyHC IIb to
MyHC IIa fibres [38].
The possible lower affinity of MyLC 3f for MyHC IIa than MyHC IIb
may be related to enhanced degradation of MyLC isoform [30]. In FT muscles stimulated with low frequency, MyLC 3f is related to an increase in the
free form on MyLC 3f, concomitant with the replacement of MyHC IIb by
MyHC IIa [39]. However, it is uncertain whether or not in all mammalian
skeletal muscles such a relationship between MyLC and MyHC isoforms is
applicable and maintained with increased or decreased contractile activities
since the stimulation-induced changes in the MyLC pattern of rabbit FT
muscles vary greatly from those of the rat [9].
Force development and shortening in muscle result from interaction of
myosin and actin. In vertebrate muscle fibres, the extent of interaction between actin and myosin is regulated by the concentration of sarcoplasmic
Ca2+. Ca2+ regulation of contraction in vertebrate striated muscle is mediated
by troponin and tropomyosin whereas striated muscles of various invertebrate species are regulated by Ca2+ binding directly to myosin [22].
Information from the crystal structure of the subfragment 1 (S1) of
skeletal muscle myosin suggests that MyLC may stabilize the α-helical
neck region of the myosin head [23] so that the force resulting from conformational changes near the active site is transmitted to the rod region
of the molecule [26]. It has been shown that the removal of up to 50 per
cent of the endogenous regulatory MyLC has little effect on either maximum Ca2+-activated force or stiffness but significantly increases force and
stiffness at submaximum levels of Ca2+ of skinned skeletal muscle fibres
[14]. In vitro force measurements [35] confirmed the results of Hofmann
et al. [14] that the removal of regulatory MyLC has little effect on maximum force. Partial extraction of regulatory MyLC from skinned skeletal
fibres indicated that it may be involved in conferring Ca2+ sensitivity on
cross-bridge transitions that limit the rate of force development in steadily
Ca2+-ac­tivated fibres [22]. In fibres containing a mutant myosin regulatory
LC having a defective divalent cation binding site, both maximum tension
and stiffness were significantly reduced compared to control values [11],
suggesting that myosin heads containing regulatory LC that is unable to
bind Ca2+ or Mg2+ have a reduced ability to form strongly bound crossbridges. These findings sug­gest that rather than playing a strictly structural
role such as stabilizing the structure of the myosin head, regulatory MyLC
may also serve a regulatory role, such as modulating the availability of
cross-bridges to bind to actin.
Two myosin LCs, one regulatory LC and one alkali LC, stabilize an extended α-helical segment in the hinge region of each MyHC. The MyLCs
are necessary for full force development [19]. Removal of either alkali or
regulatory LC markedly reduces myosin velocity in vitro motility assay [20].
Like the other contractile proteins, the alkali MyLCs represents a family of
isoforms. Five alkali MyLC isoforms have been found in human skeletal
muscle: embryonic alkali LC that is mainly expressed in embryonic muscle
tissue, a major and minor slow isoform, and two fast isoforms alkali LC1f
and LC3f, which are both encoded on the same gene. Alkali MyLC isoforms
can bring forward different contractile properties on a given MyHC [27]. The
alkali MyLCs are expressed in a fibre-type specific manner. In adult human
10
skeletal muscle, FT fibres contain fast MyLC, whereas ST fibres contain alkali
MyLC 1s and variable amounts of the two fast alkali MyLCs [16].
Role of myosin in muscle fibres shortening velocity
The MyHC isoform composition of individual muscle fibre is the primary
determinant its maximal shortening velocity and power output, while the
MyLC isoform complement has a modulatory influence in regulating these
properties [7]. It is generally accepted that the maximum velocity of shortening correlates with the MyHC isoform, several observations suggest an
additional impact of the alkali light chain complement. Several studies sug­
gest that alkali MyLCs also have a role in determining maximum velocity
of shortening [4, 13, 18, 34].
Difficulties in establishing a relation between maximum shortening velocity and myosin isoforms are caused by the preferential association between MyLC 3f and MyHC IIb and between MyLC 1f and MyHC IIa [38].
The question whether the functional significance of variations in the relative
concentration of LC3f has been adressed by several authors. The maximum
contraction velocity of a single type I fibre is approximately one tenth that of
type IIX fibre. The velocity of type IIA fibres is somewhere between those
of type I and type IIX. Although the maximum velocity of shortening correlates with both MyHC and alkali MyLC isoforms, several authors suggest
an additional impact of regulatory MyLC [17, 21]. In vitro motility assay indicates that the removal of a regulatory LC evokes a pronounced decline in
the velocity of actin filaments on myosin [20, 35]. The role of regulatory LC
in shortening velocity is supported by a single fibre study on human muscle
[17]. A role of MyLC 3 in maximum shortening velocity was suggested by
the findings that maximum shortening velocity is higher fibres containing
larger amounts of MyLC 3f [4, 7]. The variability of maximum shortening
velocity observed in type II fibres is interpreted to be attributable primarily
to differences in the alkali MyLC complements.
IIB fibres, in fact, could be faster than IIA fibres, not because they contained MyHC IIb, but because they contained larger amounts of MyLC 3f
and vice versa [7]. To address this problem, it is necessary to relate maxi-
11
mum shortening velocity to the alkali MyLC ratio in single fibre containing
only one known MyHC isoform. The only paper that followed this approach
[17] had to deal not only with the inability to separate all three fast MyHC
isoforms but also with the problem that the human fast fibres showed coexistence of two of regulatory MyLC isoforms (MyLC 2f and MyLC 2s).
Under these circumstances, no relationship between maximum shortening
velocity and alkali MyLC ratio was found either in IIA or in IIB fibres.
Undetected MyHC co existence and variations in the alkali MyLC isoform
ratio might form the basis for the large variability of maximum shortening
velocity among fast fibres presumed to contain the same fast MyHC isoform
[5, 8, 17].
It seems established that the high variability of maximum shortening
velocity in fibres with the same MyHC content can fully account for alkali MyLC composition, that is the higher the MyLC 3f content the greater the maximum shortening velocity [6, 7]. However, in human fibres, the
same considerable variability in shortening velocity cannot be satisfactorily
explained on the basis of MyLC isoform content. Alkali MyLC and regulatory MyLCs have no or hardly any role in explaining the variability in
maximum shortening velocity independently of MyHC isoforms in normal
physiological conditions. So far the findings show that it is unlikely that the
whole variability in shortening velocity observed in human muscle fibres
depends on MyLC content. The wide scattering of the relative concentration
of LC3f within fibre types IIB, IID, and IIA indicated the existance of fibres
identical by their myosin heavy chain complement, but differing their fast
LC-based isomyosins. Differences in the fractional expression or the relative
concentration of LC3f are of special interest with regard to the fact that LC3f
and LC1f are both encoded by the same gene, although their trancription
is under control of two specific promoters. The variable concentration of
LC3f within each of the three fast fibre populations points to an independent
regulation or to the existence of different thresholds of the two promoters
toward a common regulatory signal. In this respect, it is interesting to note
that the MyHC isoform, which seems more sensitive to alkali MyLC modulation in the rat, that is MyHC IIb, is not present in human skeletal muscle.
This might partly explain why alkali LC has not been shown to significantly
affect shortening velocity in human fibres [3].
12
In some studies, maximal shortening velocity was also affected by the
ratio of MyLC 3/MyLC 1f [5, 34]. However, Larsson and Moss [17] found
no relationship between MyLC 3/MyLC 1f and in human. In rodent muscle,
MyLC 3/MyLC 2f content varied significantly among a population of fibres
that expressed only the IIB MyHC isoform and greater values of MyLC 3/
MyLC 2f were associated with increased maximum shortening velocity [4].
The maximal shortening velocity of fast-twitch fibres increase with decreasing LC1f/LC3f ratios. In IIA fibres the LC1/LC3 ratio is higher than in
IIB fibres, but it is not entirely clear which subunits determine the contractile characteristics. Thus, although preliminary data showed differences in
the unloaded shortening velocity of rabbit tibialis muscle fibres depending
on whether they contain IIa or IIb MyHC isoform, these fibres also differed
in their LC1/LC3 ratio [34]. It has been shown that the unloaded shortening
velocity of rabbit soleus muscle fibres containing both type I and type IIa
MyHC isoforms was related to their ratio. Until now it has been impossible to ascribe a role only to the MyLC of mammalian skeletal muscle.
Phosphorylation of the regulatory LC alters the force-calcium relationship
but has no clear effect on shortening velocity [33, 34]. Most studies have
examined the possible role of the two alkali LC heterogeneity of myosin
by measuring ATPase activity in vitro. In view of these findings, one may
assume that LC3f is characterized by a lower affinity for MyHC I isoform
than for MyHC IIa, IId(x), and IIb isoforms. It is likely that in ST fibres
are composed solely of MyHC I isoform but the majority of the translated
MyLC 3f exists in free form [40].
Although the MyLC does not seem to affect the actin-activated myosin
ATPase activity, it has a significant impact on the shortening velocity [21].
This influence is of interest in view of the existence of various isomyosins.
The existence of two fast alkali MyLCs (LC1f, LC3f) generates three combinatorial patterns – a MyLC 1 homodimer, a MyLC 1/ MyLC 3 heterodimer, and a MyLC 3 homodimer. Their combination with a pair of regulatory
MyLC and a MyHC homodimer results in three electrophoretically distinct
isomyosins. Obviously, the number of isomyosins increases in hybrid fibres
especially by coexistence of fast and slow MyLC isoforms in combination
with MyHC isoforms.
13
References
1. Baldwin KM, Haddad F. Plasticity in skeletal cardiac, and smooth muscle.
Invited review: Effect of different activity and inactivity paradigms on myosin heavy chain gene expression in studied muscle. J Appl Physiol 2001, 90:
345–357.
2. Bicer S, Reiser PJ. Myosin light chain isoform expression among single mammalian skeletal muscle fibers: species variations. J of Muscle Res and Cell
Motolity 2004, 25: 623−633.
3. Bottinelli R. Functional heterogeneity of mammalian single muscle fibres: do
myosin isoform tell the whole story? Eur J Physiol 2001, 443: 6−17.
4. Bottinelli R, Betto R, Sciaffino S, Reggiani C. Maximum shortening velocity
and coexistance of myosin heavy chain isoforms in single skinned fast fibres of
rat skeletal muscle. J Mus Res Cell Motil 1994a, 15: 413−419.
5. Bottinelli R, Betto R, Sciaffino S, Reggiani C. Unloaded shortening velocity
and myosin heavy chain and alkali light chain isoform composition in rat skeletal muscle fibres. J Physiol (Lond) 1994b, 478: 431−449.
6. Bottinelli R, Reggiani C. Force-velocity properties and myosin light chain
isoform composition of an identified type of skinned fibres from rat skeletal
muscle. Pflügers Arch. 1995, 429: 592–594.
7. Bottinelli R, Reggiani C. Human skeletal muscle fibers: molecular and functional diversity. Progress in Biopsyhs And Mol Biol 2000, 73: 195−262.
8. Bottinelli R, Schiaffino S, Reggiani C. Force-velocity relations and myosin
heavy chain isoform compositions of skinned fibres from rat skeletal muscle.
J Physiol 1991, 437: 655–672.
9. Bär A, Simoneau JA, Pette D. Altered expression of myosin light-chain isoforms in chronically stimulated fast-twitch muscle of the rat. Eur J Biochem
1989, 178: 591–594.
10.Demirel HA, Powers SK, Naito H, Hyghes M, Coombes JS. Exercise-induced alterations in skeletal muscle myosin heavy chain phenotype: dose-response relationship. J Appl Physiol 1999, 86: 1002–1008.
11. Diffee GM, Greaser ML, Reinach F, Moss RL. Effects of non-divalent cation
binding mutant of myosin regulatory light chain on tension generation in skinned skeletal muscle fibres. Biophys J 1995, 68: 1443–1452.
12. Diffee GM, McCue S, LaRosa A, Herrick RE, Baldwin KM. Interaction of
various mechanical activity models in regulation of myosin heavy chains isoform expression. J Appl Physiol 1993, 75 (5): 2517–2522.
14
13.Greaser ML, Moss RL, Reiser PJ. Variations in contractile properties of rabbit single muscle fibres in relation to troponin-T isoforms and myosin light
chain. J Physiol 1988, 406: 85–89.
14. Hofmann PA, Metzger JM, Greaser ML, Moss RL. Effects of partial extraction of light chain 2 on the Ca2+ sensitivities of isometric tension, stiffness, and
velocity of shortening in skinned skeletal muscle fibres. J Gen Physiol 1990,
96: 477–498.
15. Hoppler H, Howald H, Conley K, Lindstedt S, Classen H, Vock P, Weibel E.
Endurance training in humans: aerobic capacity and structure of skeletal muscle. J Appl Physiol 1985, 59: 320–327.
16. Jostarndt K, Puntschart A, Hoppeler H, Billeter R. Fibre type specific
expression of essential (alkali) myosin light chains in human skeletal muscles.
J Histochem Cytochem 1996, 44: 1141–1152.
17.Larsson L, Moss RL. Maximum velocity shortening in relation to myosin isoform composition in single fibres from human skeletal muscle. J Physiol Lond
1993, 472: 595–614.
18. Li X, Larsson L. Maximum shortening velocity and myosin isoforms in single
muscle fibers from young and old rats. Am J Physiol 1996, 270: C352−360.
19. Lowey S, Trybus KM. Role of skeletal and smooth muscle myosin light chains.
Biophys J 1995, 68: 120s–127s.
20.Lowey S, Waller GS, Trybus KM. Function of skeletal muscle myosin heavy
and light chain isoforms by an in vitro mobility assay. J Biol Chem 1993a, 268
(27): 20414–20418.
21.Lowey S, Waller GS, Trybus KM. Skeletal muscle myosin light chains are
essential for physiological speeds of shortening. Nature 1993b, 365: 454–456.
22.Metzger JM, Moss RL. Myosin light chain 2 modulates calcium-sensitive
cross-bridge transitions in vertebrate skeletal muscle. Biophys J 1992, 63: 460–
468.
23.Patel JR, Diffee GM, Moss RL. Myosin regulatory light chain modulates the
Ca2+ dependence of kinetics of tension development in skeletal muscle fibres.
Biophys J 1996, 70: 2333–2340.
24. Pette D, Henriksson J, Emmerich M. Myofibrillar protein patterns of single
fibres from adult human muscle. FEBBS Lett 1979, 103: 152–155.
25.Pette D, Staron RS. Cellular and molecular diversities of mammalian skeletal
muscle fibres. Rev Physiol Biochem Pharmacol 1990, 116: 1–76.
26. Rayment JW, Rypniewski WR, Schmidt-Bäse K, Smith R, Tomchick DR,
Benning MM, Winkelmann DA, Wesenberg G, Holden HM. Three-dimensional structure of myosin subfragment-1: a molecular motor. Science 1993,
261: 50–68.
15
27. Schiaffino S, Reggiani C. Myosin isoforms in mammalian skeletal muscle.
J Appl Physiol 1994, 77: 493–501.
28.Seene T, Alev K, Kaasik P, Pehme A, Parring AM. Endurance training: volume dependent adaptational changes in myosin. Int J Sports Med 2005, 26:
815−821.
29.Seene T, Kaasik P, Alev K, Pehme A, Riso EM. Composition and turnover
of contractile proteins in volume – overtrained skeletal muscle. Int J of Sports
Medicine 2004, 25: 438–445.
30.Seene T, Kaasik P, Pehme A, Alev K, Riso EM. The effect of glucocorticoids
on the myosin heavy chain isoforms’ turnover in skeletal muscle. Journal of
Steroid Biochemistry & Molecular Biology 2003, 86 (2): 201–206.
31. Seene T, Umnova M. Relations between the changes in the turnover rate of
contractile proteins, activation of satellite cells and ultra-structural response of
neuromuscular junctions in the fast-oxidative-glucolytic muscle fibres in endurance trained rats. Journal of Basic and Applied Myology 1992, 2 (1): 34–46.
32. Seene T, Umnova M, Kaasik P. The Exercise myopathy. In: Overload,
Performance Incompetence, and Regeneration in Sport. Edited by M. Lehmann
et al. Kluwer Academic Plenum Publishers, NY, 1999, 119–130.
33. Sweeny HL, Bowman BF, Stull J. Myosin light chain phosphorylation in vertebrate striated muscle: regulation and function. Am J Physiol 1993, 264 (Cell
Physiol 33): C 1085–C 1095.
34. Sweeny HL, Kushmerick MJ, Mabuchi K, Srèter AF, Gergely J. Myosin
alkali light chain and heavy chain variations correlate with altered shortening
velocity of isolated skeletal muscle fibres. J Biol Chem 1988, 263 (18): 9034–
9039.
35. van Buren PG, Waller GS, Harris DH, Trybus KM, Warshaw DM, Lowey S.
The essential light chain is required for full force production by skeletal muscle
myosin. Proc Natl Acad Sci USA 1994, 91: 12403–12407.
36. Viru A, Viru M. Nature of training effect. In: Rarrett W.E., Kirkendale D.T.
(eds), Exercise and Sport Science 2000, 67–97.
37. Wada M, Inashima S, Yamada T, Matsunaga S. Endurance training-induced
changes in alkali light chain patterns in type IIB fibers of the rat. J Appl Physiol
2003, 94: 923−929.
38. Wada M, Pette D. Relationships between alkali light-chain complement and
myosin heavy chain isoforms in single fast-twitch fibres of rat and rabbit. Eur J
Biochem 1993, 214: 157–161.
39. Wada M, Katsuta S, Doi T, Kuno S. Favourable associations between the
myosin heavy-chain and light-chain isoforms in human skeletal muscle.
Pflügers Arch 1990, 416: 689–693.
16
40. Wada M, Okumoto T, Toro K, Masuda K, Fukubayashi T, Kikushi K,
Neihata S, Katsuta S. Expression of hybrid isomyosins in human skeletal
muscle. Am J Appl Physiol 1996, 271 (Cell Physiol 40): c1250–C1255.
41. Wahrmann JP, Winand R, Riu M. Plasticity of skeletal muscle in endurancetrained rats (I). A quantitative study. Eur J Appl Physiol 2001, 84: 367−372.
42. Whalen R, Sell S, Butler-Browne G, Schwartz K, Bouveret P, PinsetHastrom I. Three myosin heavy chain isozymes appear sequentially in rat
muscle development. Nature 1981, 292: 805–809.
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Acta Academiae Olympiquae Estoniae Vol. 14 No. 1/2, pp 18–24, 2006
IS STRENGTH TRAINING IN SPORT
CENTRE AN AEROBIC ACTIVITY?
Toomas Karu¹, Ants Nurmekivi², Jaan Loko², Tõnis Saag¹
¹Vomax OÜ
²University of Tartu, Institute of Sport Pedagogy and Coaching
Abstract
The examination of athletes with stepwise increasing loads on an ergometer
or a treadmill mostly show heart rates on an anaerobic threshold in the range
of 160–180 beats per minute, measured with the methods of gas analysis
and blood lactate concentration analysis. Persons training strength in sport
centres claim that this is a pure aerobic activity, since the heart rate measured with sport tester is usually 120–140 beats per minute. This study aims at
providing an analysis of the physiological effects produced in the organism
by usually practiced strength-type training programme in a sport centre. The
subjects investigated were two individuals who had been training in a fitness
centre for a long period of time. Each exercise was performed 10 times; an
exercise series comprised a four-fold repetition of this 10-fold exercise. During
the whole training session the heart rate of the sportsmen was measured with
sport tester, after each series of exercises a fingertip blood sample was taken
to measure lactate concentration. After each exercise series the sportsmen
were asked to evaluate on a 10-point scale, how difficult it had been for
them to perform the series.
Conclusion. Strength exercises performed by fitness sportsmen in a sport
centre produce a strong acidosis effect, as they are essentially of an anaerobic character. Simultaneously, relatively small changes occur in the heart
rate even in the case of a subjectively very strenuous strength training.
Key words: strength training, heart rate, lactate, intensity.
18
Introduction
The testing of athletes with gradually increasing loads on ergometer or treadmill reveals in most cases heart rate indices on the anaerobic threshold level
in the range of 160–180 beats per minute, measured with the methods of
gas analysis and blood lactate concentration analysis [1]. Persons training
strength in a sport centre claim that this is a pure aerobic activity, since the
heart rate measured with sport tester is usually 120–140 beats per minute.
Aim and method
This study aims at providing an analysis of the physiological effects produced in the organism by a typical strength-type training programme in a
sport centre.
The subjects investigated were two individuals who had been training
in a fitness centre for a long period of time (K. T., aged 25, 183 cm, 82 kg,
4-year sports centre training record, and A. N., aged 40, 173 cm, 88 kg,
11-year sports centre training record). The set of exercises performed on a
regular basis included: 1) squat, 2) deadlift, 3) bench press, 4) lat pulldown,
5) standing barbell curl, 6) hanging leg rise. Each exercise was performed
10 times; an exercise series comprised a four-fold repetition of this 10-fold
exercise. There were 2-minute intervals between the series and 5-minute intervals between the different types of exercises. It always took about
20 seconds to perform each exercise 10 times. The sportsmen selected loads
in accordance with their experience so that an exercise could be done 10 times. During the whole training session (85 minutes), the heart rate of the
sportsmen was measured with sport tester (Polar Vantage NV, Polar Electro,
Finland); after each series of exercises a fingertip blood sample was taken to
measure lactate concentration (Arcray Pro, Japan). After each exercise series the sportsmen were asked to evaluate on a 10-point scale, how difficult it
had been for them to perform the series. In addition, the apparent symptoms
of either fatigue or being active, and the respective response were registered.
Heart rate values were recorded with the Polar interface and software, the
final analyses were made with the Karu-Slavin Lactate programme [2].
19
Results
The loads selected by the subjects were the following (selected load / individual load record, kg):
A. N.: 1. 140/210, 2. 165/230, 3. 125/180, 4. 72/114, 5. 42/60;
K. T.: 1. 80/110, 2. 90/140, 3. 80/110, 4. 60/85, 5. 30/45.
The figures below show values obtained from the two individuals by
using the Lactate programme.
Figure 2. Training data for K. T.; symbols are identical to those in Figure 1.
The data for K. T. show a relatively good fitness level, though not as good as
that of A. N.
Figure 1. Training data for A. N.; symbols: a curve in black – heart rate, a
curve upper – computer-simulated continuous blood lactate concentration,
horizontal lines – blood lactate concentration scale as 1÷10 from low to high,
vertical lines – fingertip blood lactate concentration (marking: bottom – time
interval between the start of analysis and test, top – lactate concentration at
the moment in mmol/l).
20
From the point of view of heart rate data, the most difficult exercises were
squat and deadlift since they accelerated the heart rate by 50–60 beats. The
heart rate level observed before the repetition was recovered within 2 min.
The pre-repetition level for both subjects was about 120 beats and at this
level was formed the subjective readiness for performing the next repetition. For example, subjective difficulty in performing deadlift was associated with ratings 6, 7, 7, 8 for K. T. and 8, 8, 9, 9 for A. N. The last two marks
in each of the series were always between 7–9 for both subjects. Lactate
concentration values were the following: for K. T. 6.8 – 8.8 – 9.7 – 11.1
– 8.0 – 8.3; the average being La 9.1 mmol/l; for A. N. the respective values were 8.9 – 18.8 – 14.8 – 13.3 – 16.0 – 8.3; average La throughout the
training session being 14.0 mmol/l. Thus both sportsmen were experiencing
a strong acidosis during the whole training session. Since the level of
4.0 mmol/l is generally accepted as the anaerobic threshold of La concentration [3], from the point of view of blood La concentration, the training can
be considered a highly anaerobic one. Surprisingly no apparent symptoms
21
of fatigue were observed: the subjects were active and cheerful throughout
the training session and no perspiration was significant. The only exception
was the deadlift series, following which lasting deep breathing was apparent
during the intervals.
It is noteworthy that the two subjects displayed differences in lactate
concentration in case of performing different exercises. A. N. had the highest La concentration during deadlift, while the same level of La for K. T.
was marked during lat pulldown. Anaerobic threshold heart rate value for
K. T. in the standing position (160 beats/min) was higher than in the horizontal position (141 beats/min). This can be associated with higher heart rate
maximal values while performing the related type of exercises. Comparison
of the La intensity during the first two and the successive four exercises
reveals significant differences in the character of La regulation. The loads
increased progressively during the first two exercises and were relatively
stable in case of the successive ones.
When performing strength exercises, it is important to consider the per­
centage of the selected load with respect to the individual record load of a
certain exercise. In this study, the following percent data were obtained:
Table 1.
Percents of loads used by persons investigated from their personal
best results
Person
Squat
Deadlift
A.N.
K.T.
66
72
70
64
Bench
press
69
72
Lat pulldown
63
70
Standing barMean
bell curl
70
67,6
66
68,6
The table shows that relative percentages compared to the individual record
of the two subjects were nearly equal. However, comparison of the absolute
values of the selected loads and the percent of K. T.’s selected loads with
respect to A. N.’s selected loads yielded the following results:
22
Table 2.
Percents of personal best results of athlete K. T. from best A. N. result
Person
Squat
Deadlift
A.N.
K.T.
%
140
80
57 %
165
90
54 %
Bench
press
125
80
64 %
Lat pulldown
72
60
83 %
Standing
barbell curl
42
30
71 %
Sum
540
340
62 %
The results show that A. N. achieved a higher fitness level than K. T.
The average heart rate during the training session for A. N. and K. T.
was 119.5 and 130.5 beats/min, respectively. Thus, it can be suggested that
though A. N. used higher loads, his training load with respect to the maximum is comparable to that of K. T. The analysis of the anaerobic threshold
for the two subjects made with the Lactate programme on the basis of the given loads showed that the results for A. N. and K. T. were 121 and 161 beats/
min, respectively. If the selected loads had been relatively equal, it would
have been possible to conclude that K. T. had a better aerobic capacity, since
his anaerobic threshold was higher and the range of lactate regulation was
lower. As a matter of fact, the absolute loads selected by A. N. were almost
twice as high as those selected by K. T.; the same can be said about blood
lactate concentration during the whole training. It can be concluded that A. N.
is better prepared for work with maximum loads at the anaerobic zone, has a
larger amount of fast muscle fibres and a higher lactate tolerance.
In case of strength exercises heart rate analyses performed without the
measurement of lactate concentration do not provide the adequate picture of
the training intensity. Lactate concentration values of the two sportsmen obtained in the course of the training session were more than 2–3 times higher
than anaerobic threshold values.
This observation implies that the measurement of strength training intensity is complicated, especially if strength exercises are involved in endurance
training. Although following strength exercises the blood lactate concentration remains above 6–7 mmol/l and pH below 7.0, sportsmen are capable of
continuing their training session [4]. These authors have noted that though
blood La level can be used as reference for supervising endurance training,
its connexion to changes in the muscle cells is not exactly known. The mea­
23
Acta Academiae Olympiquae Estoniae Vol. 14 No. 1/2, pp 25–37, 2006
surements of La characterize the La regulation level of an individual well,
even if made only during one training session. Yet they can be administered
only for elite athletes because of the complexity of the tests.
Summary
Strength exercises used by fitness sportsmen in sport centre produce a strong acidosis effect, as they are essentially of an anaerobic character.
Simultaneously relatively small changes occur in heart rate even in case of
subjectively strenuous power training, which may be misleading for both
the coach and the sportsmen. Intensive strength training compared to endurance training seems to be easy, judging by heart rate indices. Adequate
evaluation of strength training intensity can be obtained only by measuring
blood lactate concentration or by asking sportsmen to give subjective evaluation of intensity rating on a 10-point scale.
References
1. Hollmann W, Hettinger T. Sportmedizin. �����������������������
Grundlagen für Arbeit,
Training und Präventivmedizin. Schattauer,
���������������������������������
Stuttgart, NY., 2000.
2. Karu T, Slavin G. Sports software Lactate. User’s Guide. Tartu, 2005.
3. McArdle WD, Katch FD, Katch VL. Exercise Physiology. Fourth edition, Williams and Wilkins, 1996.
4. Wilmore JH, Costill DL. Physiology of Sport and Exercise. Human
Kinetics, Champaign, Il, 1994.
Twitch contractile properties of
plantarflexor muscles in Nordic combined
athletes and cross-country skiers
Jaan Ereline, Helena Gapeyeva, Mati Pääsuke
Institute of Exercise Biology and Physiotherapy, University of Tartu,
Tartu
Abstract
The purpose of this study was to compare twitch contractile properties of skeletal muscles in male athletes who train power and endurance simultaneously
(Nordic combined athletes) and athletes who train endurance (cross-country
skiers). To determine the contractile properties of plantar­flexor muscles during isometric twitch, the posterior tibial nerve in popliteal fossa was stimulated by supramaximal square wave pulses of 1-ms duration. Twitch peak force
(PF), contraction (CT) and half-relaxation (HRT) times were measured. The
percentage increase in twitch PF after maximal voluntary contraction (MVC)
of 5-s duration in relation to resting twitch was taken as an indicator of postactivation potentiation (PAP). Twitch PF:MVC force ratio was also calculated.
Nine Nordic combined athletes and 12 cross-country skiers aged 19–26 years
participated in the study. Twitch PF and PF:MVC did not differ significantly
in Nordic combined athletes and cross-country skiers. Nordic combined athletes had a significantly (p < 0.05) greater PAP as compared to cross-country
skiers. Cross-country skiers had a significantly (p < 0.05) greater CT and HRT
compared to Nordic combined athletes.
Twitch contractile properties of plantarflexor muscles did not differ (PF,
PF:MVC) markedly in athletes who train power and endurance simultaneously in comparison with athletes who predominantly train endurance.
Long-term simultaneous power and endurance training induced increase in
twitch potentiation capacity and the shortening of contraction and relaxation
times of plantarflexor muscles.
Key words: human plantarflexor muscles, muscle force, isometric contraction, twitch contraction.
24
Introduction
It is well known that exercise training can induce different adaptation processes in the neuromuscular system through changes in the neural control as
well as morphology of the skeletal muscles. Several longitudinal studies
have shown structural muscle modifications, such as changes in contractile proteins expression [18], and neural adaptations, such as alterations in
motor units activation [8] or decreased antagonist co-contraction [5] after
the performance of different training programmes. Nevertheless, to analyze
human long-term training adaptations, preferentially cross sectional studies
have been used. Some of these experiments have focused on analyzing the
differences in neuromuscular system of power-trained and endurance-trained athletes [15, 16, 20], illustrating that systematic exercise training tends
to induce specific adaptation processes of neuromuscular system in relation
to the type of physical activity performed.
The measurement of twitch contractile properties of athlete’s muscles
has been used for the analysis of specificity adaptation of the neuromuscular
system to various types of systematic training [2, 24, 29]. By using electrically evoked supramaximal isometric twitch characteristics, the contractile
properties of human skeletal muscles can be determined independently from
the control and activation by the nervous system. Twitch contractile properties have been shown to differ in heavy resistance-trained athletes compared
to sedentary subjects [28] and in power-trained athletes compared to endurance-trained athletes and sedentary subjects [20, 25]. Previous studies
performed in our laboratory indicated that power training induces a more
evident increase of force-generating capacity and speed of contraction and
relaxation in plantarflexor muscles than endurance training [25]. Similar results have been obtained by other authors [1]. However, no studies have
investigated twitch contractile properties of skeletal muscles in athletes who
combine power and endurance training simultaneously as is the case with
Nordic combined athletes.
Twitch contraction force is increased after a brief maximal voluntary
contraction (MVC). This enhancement is called post-activation potentiation (PAP) [4, 21]. The most accepted mechanism underlying PAP is a phos­
phorylation of myosin regulatory light chains during the conditioning cont-
26
raction, which renders actin-myosin more sensitive to Ca2+ in subsequent
twitch [9, 31, 32]. Only one cross-sectional study has been surveyed in
which PAP has been assessed in endurance-trained athletes [12]. The results
showed that twitch PAP for the muscles trained was greater in power and
endurance-trained athletes than only endurance-trained athletes, suggesting
that the enhanced PAP in endurance athletes was more likely the result of
training adaptations than genetic endowment. Nevertheless, little it is known
about the influence of simultaneous power and endurance training on twitch
potentiation capacity of human skeletal muscles.
The purpose of this study was to compare the electrically evoked twitch
contractile characteristics of skeletal muscles at rest and PAP of twitch
force in elite male athletes, who train power and endurance simultaneously
(Nordic combined athletes) and athletes who train predominantly endurance
(cross-country skiers). Plantarflexor muscles which are involved in many
working and sports activities, including power and endurance events, were
tested.
Material and Methods
Subjects. Three groups of subjects were studied: Nordic combined athletes (n = 9) and cross-country skiers (n = 12). The athletes were members
of Estonian national teams. Their training experience was 7–11 years. All
subjects were informed of the procedures and the purpose of the study and
their written informed consent was obtained. The study carried the approval
of the University Ethics Committee for human studies. The anthropometric
characteristics of the subjects are presented in Table 1.
27
Table 1.
Anthropometric data, maximal voluntary contraction (MVC) force of
the plantarflexor muscles and MVC force relative to body mass (MVC
force:BM) in athletes (mean ± SE)
Variables
Age (ys)
Height (cm)
Body mass (kg)
Body mass index (kg⋅m-2)
MVC force (N)
MVC force:BM (N⋅kg-1)
Groups
Nordic combined
athletes (n = 9)
22.1 ± 1.1
179.3 ± 1.3
70.2 ± 1.5
21.1 ± 0.3
1112 ± 39
15.7 ± 0.3
Cross-country
skiers (n = 12)
24.1 ± 1.2
179.9 ± 1.8
72.2 ± 1.4
22.1 ± 0.4 *
1041 ± 26 *
14.3 ± 0.4 *
* p < 0.05 compared with Nordic combined athletes
Testing procedures. During the experiment the subjects were seated on a
custom-made dynamometer chair with the dominant leg (usually the right leg)
flexed 90 deg at the knee angle and mounted inside a metal frame [22]. The
foot was strapped to an aluminium foot plate. The inclination of the foot could
be altered by rotating the footplate about an axis that corresponded to that of
the ankle joint, i.e. the medial malleolus. The ankle was dorsiflexed to 20 deg.
This angle was associated with maximal voluntary and stimulated torques and
presumably corresponded to the “optimal” muscle length [27]. The kneecap
and front side of the thigh were held down by an adjustable pad. Torques
acting on the footplate were sensed by a standard strain-gauge transducer connected with the footplate by rigid bar. The electrical signals from the straingauge transducers were amplified and displayed with a special amplifier. The
system was linear from 10 to 1600 N. The point of application of force to the
footplate was located on articulation regions between the metatarsus and ossa
digitorum pedis. The force signals were sampled at the frequency of 1 kHz
and stored on a hard disk for further analysis.
To determine the contractile properties of the plantarflexor muscles during isometric twitch, the posterior tibial nerve was stimulated through a pair
of 2 mm-thick, self-adhesive surface electrodes (Medicompex SA, Ecublens,
28
Switzerland). Prior to attaching the stimulating electrodes, electrode gel was
applied to the contact surface, and the underlying skin was prepared by shaving, sanding and rubbing with isopropyl alcohol. The cathode (5 x 5 cm)
was placed over the tibial nerve in popliteal fossa and anode (5 x 10 cm)
was placed under the posterior-medial side of the thigh. Supramaximal square
wave pulses of 1-ms duration were delivered from an isolated voltage stimulator Medicor MG-440 (Budapest, Hungary). The evoked compound action
potential (M-wave) of the soleus muscle was recorded using bipolar (20 mm
interelectrode distance) electromyogram (EMG) electrodes (Beckman miniature skin electrodes). The electrodes were placed longitudinally on the belly of
the soleus muscle after the skin was cleaned using alcohol swabs and abraded
lightly with fine sand paper. As a reference electrode a self-adhesive surface
electrode (Medicompex SA, 5 x 10 cm) was placed over the proximal part of
the triceps surae muscle between the stimulating and recording electrodes.
The EMG signals were amplified and displayed using a standard Medicor
MG-440 (Budapest, Hungary) preamplifier with the frequency band ranging
from 1 Hz to 1 kHz. These signals were sampled at 1 kHz.
On reporting to the laboratory, the subject sat resting for about 25 min before
the dominant leg was placed in the apparatus. The rest period minimized any
potentiation effect from walking to the laboratory. A maximal resting twitch was
elicited by delivering a series of single stimuli of increasing intensity until theplateau of M-wave amplitude was obtained. During isometric twitch recording
the stimulus intensity varied from approximately 25 V to sup­ramaximal in increments of 50% (130–150 V). Firstly, three supramaximal isometric twitches of the
plantarflexor muscles were elicited. Two minutes after the last resting twitch was
recorded, the subjects were instructed to make a MVC for 5 s and then to relax.
Postactivation twitch was elicited within 2 s after the onset of relaxation. Two
minutes after the postactivation twitch was recorded, subjects performed three
isometric MVCs of the plantarflexor muscles. The joint position was the same
as for previous twitch measurements. The subjects were instructed to push the
footplate as forcefully as possible for 2–3 s. Strong verbal encouragement and visual feedback were used to motivate the subjects. The greatest force of the three
maximal efforts was taken as the isometric MVC force. Two-minute rest periods
were allowed between trials. Skin temperature of the tested muscle group was
continuously controlled and maintained at 35 ºC with an infrared lamp.
29
The following characteristics of resting isometric twitch were calculated:
peak force (PF) – the highest value of isometric force production; contraction time (CT) – the time to twitch maximal force; half-relaxation time
(HRT) – the time of half of the decline in twitch maximal force. The percentage increase in postactivation twitch PF in relation to resting twitch was
taken as an indicator of PAP. Twitch PF was expressed as a ratio to MVC.
The MVC force was calculated in relation to body mass of the subjects.
Statistics. Data are means and standard errors (± SE). One-way analysis of
variance (ANOVA) followed by Scheffe post hoc comparisons were used to
test for differences between groups. Pearson correlation was used to observe
the relationship between PAP of twitch force, and resting twitch CT and HRT.
A level of p < 0.05 was selected to indicate statistical significance.
Table 2 provides the correlation coefficients between twitch PAP, and resting
twitch CT and HRT in Nordic combined athletes and cross-country skiers.
In cross-country skiers twitch PAP correlated negatively (p < 0.05) with resting twitch CT (r = –0.66, p < 0.05). No significant correlations (p > 0.05)
were found between twitch PAP and time-course characteristics of resting
twitch in Nordic combined athletes.
Results
The body mass of Nordic combined athletes and cross-country skiers did not
differ significantly (Table 1). The body mass index (BMI) was significantly less in Nordic combined athletes compared with cross-country skiers
(p < 0.05) (Table 1). Nordic combined athletes had a significantly (p < 0.05)
greater MVC and MVC force relative to body mass as compared with crosscountry skiers.
Table 2.
Correlation coefficients between postactivation potentiation (PAP) of
twitch peak force (PF) and resting twitch contraction (CT) and halfrelaxation (HRT) times in Nordic combined athletes (NCA) and crosscountry skiers (CCS).
PF
CT
HRT
* p < 0.05
30
NCA
0.47
0.36
0.14
PAP
CCS
0.51
– 0.66 *
0.34
Figure 1. Twitch peak force (PF) (A) and peak force related to maximal
voluntary contraction force (PF:MVC) (B), and postactivation potentiation
(PAP) (C) in Nordic combined athletes (NCA, n = 9) and cross-country
skiers (CCS, n = 12). Mean ± SE
* p < 0.05
Twitch PF and PF:MVC did not differ significantly in the measured groups
(Fig. 1A, 1B). Nordic combined athletes had greater (p < 0.05) twitch PAP
compared with cross-country skiers (Fig. 1C). Twitch CT and HRT were
31
shorter in Nordic combined athletes (p < 0.05) compared with cross-country
skiers (Fig. 2).
Figure 2. Twitch contraction time (CT) (A) and half-relaxation time (HRT)
(B) in Nordic combined athletes (NCA, n = 9) and cross-country skiers
(CCS, n = 12). Mean ± SE
* p < 0.05
Discussion
To investigate whether long-term simultaneous power and endurance training
induces differences in electrically evoked twitch contractile characteristics
of plantarflexor muscles in comparison with long-term endurance training,
elite Nordic combined athletes and cross-country skiers were compared.
The main findings of this study were that: (1) twitch contractile properties
(PF, PF:MVC) of plantarflexor muscles did not differ significantly in Nordic
combined athletes and cross country skiers; (2) Nordic combined athletes
had higher twitch PAP and shorter resting twitch CT and HRT compared to
cross-country skiers.
It has been hypothesized that Nordic combined athletes have a greater
evoked twitch force-generating capacity in plantarflexor muscles than crosscountry skiers. Nordic combined includes two different sports events – ski
jumping and cross-country skiing – and the athletes must combine strategies
of both disciplines into one training schedule. Training in Nordic combined
32
requires special explosive-type strength (power) exercises in combination
with endurance exercises for lower extremities. Higher twitch PF in powertrained athletes compared to endurance-trained athletes and sedentary subjects has been previously reported [16, 20, 25]. Several factors can contribute to the increase twitch force in power-trained athletes’ muscles. High
level power-trained athletes have a greater number of fast twitch fibres in
their muscles than endurance trained athletes [6]. Some studies have shown
selective hypertrophy of fast twitch fibres after systematic strength/power
training [1, 21]. It has also been suggested that longitudinal power training
causes changes in excitation-contraction coupling and contractile apparatus
of the muscle fibres which can affect their force generating capacity [7].
However, contrary to our hypothesis, no significant differences were observed in twitch PF between Nordic combined athletes and cross-country
skiers. In this regard, several concurrent training studies have shown simultaneous strength/power and endurance training inhibiting muscle force
production capacity when compared with strength/power training alone
[17]. This could partly explain the similarly evoked twitch force observed in
Nordic combined athletes and cross-country skiers.
One indicator of muscle contractile properties is the twitch:tetanus ratio.
MVC force is similar to maximal force of tetanically evoked contractions in
human muscles [3] and therefore we calculated twitch PF:MVC force ratio.
Nordic combined athletes did not have any significant differences in twitch
PF:MVC force ratio compared to cross-country skiers, suggesting higher
voluntary muscle activation capacity. In fast muscles, the twitch:tetanus ratio is smaller compared with slow muscles [10]. It has been suggested that
the smaller twitch:tetanus ratio in power-trained athletes can be related to a
larger cross-sectional area in their muscles [19].
The isometric twitch force production can be enhanced by preceding contractile activity, such as occurs with PAP. The results of the present study
showed that twitch PAP was ���������������������������������������������
significantly��������������������������������
greater in Nordic combined athletes than cross-country skiers. ����������������������������������������������
Our previous studies indicated greater twitch
PAP in plantarflexor muscles in power-trained athletes (sprinters and jumpers)
compared to endurance-trained athletes (long-distance runners) and sedentary
subjects [23, 25, 30]. Hamada et al. [12] observed that the magnitude of twitch
PAP was increased in endurance and strength-trained athletes in comparison
33
to sedentary subjects only for the trained muscles, suggesting that PAP enhancement could be explained by specific neuromuscular adaptation induced
by training.���������������������������������������������������������������
Power training can enhance twitch PAP by increased ability to
activate the muscles during MVC used induce PAP. Increased ability to activate high threshold motor units consisting of fast-twitch muscle fibres should
increase twitch PAP because fast-twitch fibres show greater PAP than slowtwitch fibres [11, 26]. PAP
�������������������������������������������������������
is often associated with a shortening of twitch CT
and HRT [11, 12]. In the present study twitch PAP was significantly negatively
correlated with resting twitch CT in cross-country skiers, whereas no significant correlations were observed between PAP and time-course characteristics of resting twitch in Nordic combined athletes. It was hypothesized that
in endurance athletes the correlation between PAP and twitch CT is predominantly influenced by training adaptations in slow-twitch muscle fibres [11].
Nordic combined athletes had significantly shorter resting twitch CT
and HRT compared to cross-country skiers. Our previous studies indicated shorter CT and HRT in power-trained athletes (sprinters and jumpers)
and endurance-trained athletes (long-distance runners) compared to sedentary subjects with no significant differences between the measured athletes’
groups [24]. On muscle fibres level the time course of isometric twitches is
probably highly dependent on the kinetics of excitation-contraction coupling mechanisms, including intracellular calcium movements [13, 14]. The
shortened twitch contraction and half-relaxation time of Nordic combined
athletes muscles noted in the present study indicates increased efficiency in
sarcoplasmatic reticulum function.
Conclusions
Long-term simultaneous power and endurance training induced increase in
twitch potentiation capacity, and the shortening of contraction and relaxation times of the plantarflexor muscles, while endurance training alone did
not induce these changes. Twitch PAP was related to resting twitch CT in
cross-country skiers, whereas no significant relationship between PAP and
34
time-course characteristics of resting twitch was observed in Nordic combined athletes.
References
1.Alway SE, MacDougall JD, Sale DG, Sutton JR, McComas A.J. Functional
and structural adaptations in skeletal muscle of trained athletes. J Appl Physiol
1988, 64: 1114–1120.
2. Alway SE, MacDougall JD, Sale DG Contractile adaptations in human triceps
surae after isometric exercise. J Appl Physiol 1989, 66: 2725–2732.
3. Bigland-Ritchie B, Johnson R, Lippold OCT, Smith S, Words JJ. Changes
in motoneuron firing rates during sustained maximal voluntary contractions.
J Physiol Lond 1983, 340: 335–346.
4. Brown IE, Loeb GE. Postactivation potentiation – a clue for simplifying models of muscle dynamics. Amer Zool 1998, 38: 743–754.
5. Carolan B, Cafarelli E. Adaptations in coactivation after isometric resistance
training. J Appl Physiol 1992, 73: 911–917.
6. Costill DL, Fink WJ, Pollock ML. Muscle fiber composition and enzyme activities of elite distance runners. Med Sci Sports 1976, 8: 96–100.
7. Duchateau J, Hainaut K. Isometric or dynamic training: differential effects on
mechanical properties of a human muscle. J Appl Physiol 1984, 56: 296–301.
8. Enoka RM. Neural adaptations with chronic physical activity. J Biomech 1997,
30: 447–455.
9. Grange RW, Vandenboom R, Houston ME. Physiological significance of
myosin phosphorylation in skeletal muscle. Can J Appl Physiol 1993, 18: 229–
242.
10. Hainaut K, Duchateau J. Neuromuscular electrical stimulation and voluntary
exercise. Sports Med 1992, 14: 100–113.
11. Hamada T, Sale DG, MacDougall JD, Tarnopolsky MA. Interaction of fibre
type, potentiation and fatigue in human knee extensor muscles. Acta Physiol
Scand 2003, 178: 165–173.
12. Hamada T, Sale DG, MacDougall JD. Postactivation potentiation in endurance-trained male athletes. Med Sci Sports Exerc 2000, 32: 403–411.
13. Klug GA, Leberer E, Leisner E, Simoneau JA, Pette D. ����������������
Relationship between parvalbumin content and the speed of relaxation in chronically stimulated rabbit fast twitch muscle. Pflügers Arch 1988, 411: 126–131.
14. Kugelberg E, Thornell LE. Conduction time, histochemical type, and terminal cisternae volume of rat motor units. Muscle Nerve 1983, 6: 149–153.
35
15. Kyröläinen H, Komi PV. Neuromuscular performance of lower limbs during
voluntary and reflex activity in power- and endurance-trained athletes. Eur J
Appl Physiol 1994, 69: 233–239.
16. Lattier G, Millet GY, Maffiuletti NA, Babault N, Lepers R. Neuromuscular
differences between endurance-trained, power-trained, and sedentary subjects.
J Strength Cond Res 2003, 17: 514–521.
17. Leveritt M, Abernethy PJ, Barry BK, Logan PA. Concurrent strength and
endurance training. Sports Med 1999, 28: 413–427.
18. Liu Y, Schlumberger A, Wirth K, Schmidtbleicher D, Steinacker JM.
Different effects on human skeletal myosin heavy chain isoform expression:
strength vs. combination training. J Appl Physiol 2003, 94: 2282–2288.
19. MacDougall JD, Sale DG, Alway SE, Sutton JR. Muscle fiber number in
biceps brachii in bodybuilders and control subjects. J Appl Physiol 1984, 57:
1399–1403.
20. Maffiuletti NA, Martin A, Babault N, Pensini M, Lucas B, Schiepatti M.
Electrical and mechanical H(max)-to-M(max) ratio in power- and endurancetrained athletes. J Appl Physiol 2001, 90: 3–9.
21. Moore RL, Stull JT. Myosin light chain phosphorylation in fast and slow skeletal muscle in situ. Am J Physiol 1984, 247: C462–C471.
22. Pääsuke M, Ereline J, Gapeyeva H, Sirkel S, Sander P. Age-related differences in twitch contractile properties of plantarflexor muscles in women. Acta
Physiol Scand 2000, 170: 51–57.
23.Pääsuke M, Ereline J, Gapeyeva H, Torop T. Twitch contractile properties
of plantarflexor muscles in female power-trained athletes. Med Sport 2002, 55:
279–286.
24. Pääsuke M, Ereline J, Gapeyeva H. Twitch contractile properties of plantar
flexor muscles in power and endurance trained athletes. Eur J Appl Physiol
1999, 80: 448–451.
25.Pääsuke M, Ereline J, Gapeyeva H. Twitch potentiation capacity of plantar­
flexor muscles in endurance and power athletes. Biol Sport 1998, 15: 171–
178.
26. Putman CT, Xu X, Gillies E, MacLean IM, Bell GJ. ������������������������
Effects of strength, endurance and combined training on myosin heavy chain content and fibre-type
distribution in humans. Eur J Appl Physiol 2004, 92: 376–384.
27.Sale DG, Quinlan J, Marsh E, McComas AJ, Belanger AY. Influence
�������������������
of joint
position on ankle plantarflexion in humans. J Appl Physiol 1982, 52: 1632–
1642.
28.Sale DG, Upton ARM, McComas AJ, Mac Dougall JD. Neuromuscular
function in weight-trainers. Exp Neurol 1983, 82: 521–531.
36
29. Sleivert GG, Backus RD, Wenger HA. Neuromuscular differences between
volleyball players, middle distance runners and untrained controls. Int J Sports
Med 1995, 16: 390–398.
30.Sweeney HL, Bowman BF, Stull JT. Myosin light chain phosphorylation in
vertebrate striated muscle: regulation and function. Am J Physiol 1993, 264:
C1085–C1095.
31.Sweeney HL, Stull JT. A���������������������������������������������������
lteration of cross-bridge kinetics by myosin light
chain phosphorylation in rabbit skeletal muscle: Implications for regulation of
actin-myosin interaction. Proc Natl Acad Sci USA 1990, 87: 414–418.
32.Yang Z, Stull JT, Levine RJC, Sweeney HL. Changes in interfilament spacing
mimic the effects of myosin regulatory light chain phosphorylation in rabbit
psoas fibers. J Struct Biol 1998, 122: 139–148.
37
Acta Academiae Olympiquae Estoniae Vol. 14 No. 1/2, pp 38–48, 2006
THE PHENOMENON OF MECHANICAL STRESS
TRANSMISSION IN SKELETAL MUSCLES
Arved Vain
Institute of Experimental Physics and Technology,
University of Tartu, Estonia
Abstract
The nature of the mechanical stress transmission in the skeletal muscle in
the motion of living organism is of principal importance. It forms the basis for understanding the mechanics of the contraction process, effective
usage of the biomechanical properties of muscles and also muscular tone
estimation. Available publications describing biomechanical models of the
skeletal muscle support the concept, that the transmission of mechanical
stress in skeletal muscle takes place along myofilaments and at the ends
of the myofilaments via special binding agent to tendons. This hypothesis
has been heavily criticized during late years. In accordance with the new
biomechanical model of the skeletal muscle the movement of the crossbridges in the process of contraction of the skeletal muscle creates a radial
force, which causes the increase of the perimeter of the muscle. So there
should exist a latency period between the skeletal muscle perimeter increase and the formation of the contraction force in muscles at their steady
state length. The existence of this latency period in case of some m. triceps
surae of rabbits has been established experimentally. It is concluded that
in the contraction of skeletal muscle the perimeter increase belongs to the
fundamental causes, not to the results of muscle contraction. The mechanical stress transmission from sarcomere to tendon takes place via complex
transmission of longitudinal and radial components of the force generated
by the myofilament cross-bridges. The radial component is transmitted via
muscle envelopes, the longitudinal component via costamere network to the
muscle envelopes.
Key words: skeletal muscle, mechanical stress transmission, biomechanical
properties.
38
Introduction
The mechanism of the mechanical energy generation and transmission to the
bone levers is one of the most complicated phenomenons of the functioning
of skeletal muscle. This mechanism is a complicated one, as the force transmission must be guaranteed even in case the skeletal muscle involved in the
process has partial mechanical injuries.
At present many important facts concerning the structure of skeletal
muscles are known, also several probable pathways of mechanical stress
transmission, but up to the moment there does not exist any conceptual understanding, covering all the aspects of this complicated phenomenon.
In the present study an attempt has been made to establish the role of
the helica of the collagen filaments situated in the endo-, peri- and epimyseum of the muscle in the process of the mechanical stress transmission
from sarcomere to tendon.
As a rule the studies in the field of the skeletal muscle biomechanics have
been based on the model of the muscle by Hill. In the model the collagen
filaments, passing directly over into tendons, are presented as a parallel elastic element (Fig. 1a).
Fig. 1. Biomechanical models of skeletal muscle. a – the traditional accepted
model of skeletal muscle, b – the new model.
If the conclusion is based on the hypothesis, stating that the mechanical
stress evoked in a sarcomere is transmitted in the longitudinal direction inside the myofibril from the force-generating sarcomere to its serial neighbour,
then in the process of muscle shortening the stiffness of endo-, peri- and epi39
myseum should decrease in comparison with their stiffness in the steady state of the muscle. The experimental data of studies dealing with the problem
prove the situation to be vice versa. The freguency of oscillation measured
by myometer [3, 7, 15, 16] of muscle envelopes increases with the increase
of contraction force (Fig. 2).
case of the muscle envelope stress increase. To test this hypothesis an experimental study (with docent E. Hietanen) was carried out at the Laboratory
of clinical physiology of the University of Turku. The natural oscillation
frequency of muscles was measured by myometer [3, 7, 15, 16] and the intramuscular pressure using the invasive wick catheter method by Stryker [1].
The results of the experiments are presented in Fig. 3.
Fig. 2. Dependence of the muscle natural oscillation frequency on the load
magnitude.
So it can be supposed that part of the force generated in sarcomere is transmitted to tendon via collagen helica of endo-, peri- and epimyseum. In favour
of this hypothesis there exist several results of experimental studies. In their
original experiment Street and Ramsey [11] established, that the sarcolemma transmits the active contraction force to the tendon. The experiments
by Fields [2] proved, that the mechanical properties of the sarcolemma are
sufficient for it to be a means for transmitting mechanical stress to tendon.
The results of Maughan and Godt [8], who established, that “... the radial
force per thick filament was 1.2·10-9 N and the longitudinal force per thick
filament 1.4·10-10 N...” are thought-provoking. Still more clear evidence
in favour of the active part of endo-, peri- and epimyseum in the process
of muscle contraction present the studies by Kirby et al. [6], Jerosch [4],
Järvholm et al. [5], who established, that the process of muscle contraction
takes place simultaneously with adequate intramuscular pressure changes.
It is clear, that the intramuscular pressure increase can take place only in
40
Fig. 3. Dependence of intramuscular pressure and muscle oscillation
frequency on the load applied to the muscle.
On the basis of the above-mentioned the hypothesis can be stated, that the
muscle perimeter increase observed in the process of muscle contraction is
not a result of the myofilament sliding process, but, on the contrary, appears
to be its fundamental cause. The results of the in vivo experiments [12],
where the force, generated by m. biceps brachii was recorded synchronically with the perimeter of the muscle, show, that the muscle perimeter increase
precedes the muscle force appearance for a time interval from (86 ± 10) to
(202 ± 19) ms, depending on the type and speed of muscular contraction.
In accordance with the new biomechanical model of skeletal muscle (Fig.
41
1b) the perimeter increase belongs to the origins, not to the results of muscle
contraction.
In the present study the results of our recent experiments using electro­
stimulation to cause contraction of the specimens of rabbit’s m. triceps surae with simultaneous recording of the changes in muscle length, perimeter
and diameter are analysed.
Methods
The experiments were carried out using the specimens of m. triceps surae
of 16 full-grown rabbits (average weight 3.933 kg). The experiment layout
included three inductive displacement probes, perimeter probe and the electrodes used in electrostimulation. The layout made it possible to give the
specimen an initial statical load (see Fig. 4). The displacement probes were
used to record the length changes of tendo calcanei, the muscle length and
diameter increase.
Experimental
Immediately before placing in the experimental apparatus the specimen
was held in physiological NaCl solution for 15 minutes. After fixing it in
the experimental apparatus the specimen was loaded with the load of 10 N
for 10 seconds. After that the specimen was submitted to electrostimulation
procedures (AC current 20 mA, cyclically – contraction for 4 s, pause 4 s).
The results were recorded using the pattern: 100 samples per secunde, 12
contractions with the load of 2 N and 15 contractions with the load of 12 N
(see Fig. 5).
Fig. 5. Perimeter and length changes during muscle contraction.
Results and discussion
Fig. 4. Experiment layout.
42
In accordance with the new biomechanical model of the skeletal muscle [12,
13] the movement of the cross-bridges in the actin-myosin complex in the
process of contraction of the skeletal muscle creates a radial force, which
causes the increase of the perimeter of the fibre, bunch of fibres and the
43
muscle as a whole. The perimeter increase precedes the muscle contraction
for (17.46 ± 1.50) ms (see Fig. 5). This fact indicates that the stress generated in a sarcomere is not transmitted from one sarcomere in series to another
only, but the radial force component, evoked in the process of the circular
movement of cross-bridges in the contraction process, is transmitted via the
stress of muscle envelopes, evoked by the skeletal muscle perimeter increase, through the collagen helica, which pass directly over into tendon, to the
tendon. As can be understood from the very thorough review of the possible
force transmission pathways from actomysin to tendon by Patel and Lieber
[10], the conclusion of the possibility of lateral force transmission is quite
convincing. It can be supposed that if in the process of this lateral force
transmission the costameres should transmit the force not to the stressed
collagen helica in endo-, peri- and epimyseum, such a force transmission
process would have very small effectivity. In accordance with the new biomechanical model of the skeletal muscle the role of the radial component of
the cross-bridge force is more important than that of the longitudinal component at the initial moment of the contraction process (see Fig. 6).
Fig. 6. Time dependence of muscle length, diameter and perimeter in muscle
contraction process, using the load of 12 N.
44
But as at the beginning of the contraction process in result of the radial
movement of the cross-bridges in relation of the myofilament the stress of
muscle envelopes and the intramuscular pressure increase are initiated [5],
after what to the muscle contraction forces via the focal adhesion sites the
longitudinal component of the cross-bridges elasticity force is added, the
universality of the phenomenon can be clearly understood. If the skeletal
muscle performs active work not only in the contraction process, but also
in the eccentric regimen, the transition from the latter to the concentric regimen and vice versa being the normal working regimen of skeletal muscles.The above-presented interpretation of the phenomenon of mechanical
stress transmission also gives explanations to many contraversities of the
muscle model by Hill. For example in case of radial force transmission it is
understandable that the myofilament length cannot increase in the process
of contraction. In other way, the pulling stress of the myofilament is significantly smaller than the pulling stress of collagen fibres in the muscle
contraction process. Also the transmission of mechanical stress at the connection of myofilament to tendon does not take place. In addition it is a wellfounded remark by Patel and Lieber [10], that “...if myofibrils are interconnected as described above, how is a new myofibril inserted? The answer
is not clear, but must involve the remodelling of the intermediate filament
network between adjacent myofibrils”. The phenomenon of the cross-bridge
force radial component, increasing the muscle perimeter, evidently makes
it possible to give the answer to the above-presented question. Also it is not
necessary to assume any more that muscle fibres generate force along all
their length and that this force is transmitted only in series to the muscletendon junction. Patel and Lieber [10] state, that “...detailed measurements
of muscle fiber lengths within intact whole muscles have revealed the seemingly paradoxical result that, in many muscles, fibers do not extend from
one tendon plate to the other ... This raises the general question as to how
muscle fiber contractile force is transmitted to an external tendon, which
may be quite a distance away from the fiber insertion site. In other words,
the concept that all muscle fibers are arranged in bundles and transmit force
along their length to the end regions, where they insert onto major tendon
plates, is no longer tenable”.
45
To explain the dependence of the force evoked in the collagen helix of
muscle fibre on the length of sarcomere in contraction and stretching caused
by external force a corresponding computer simulation study was performed. The results of the computer simulation show that in accordance with
the new model [12, 13] of skeletal muscle the strain of collagen fibres in
contraction process is determined (see Fig. 7) by the perpendicular component FE┴ and during the stretching by an external force FE by the longitudinal
component FE║ [14].
the muscle envelopes, using the mechanisms of perpendicular as well as
lateral force transmission.
As a conclusion from the above mentioned discussion, efficiency of the
mechanical stress transmission from the sarcomere to bone levers depends
on skeletal muscle tone and biomechanical properties of muscle envelopes
– stiffness and elasticity.
Acknowledgements
The study has been carried out at the Department of Forensic Medicine of
the University of Helsinki and has been supported by prof. A. Penttilä and
prof. E. Vuori
References
Fig. 7. Dependence of the muscle fibre element elasticity force FE on the
length of the element L.
Conclusions
The mechanical stress generated in the actin-myosin complex of the sarcomere of skeletal muscle is transmitted from its generation place to tendon
via the collagen helica, situated in the endo-, peri- and epimyseum of the
muscle. The radial component of the force, generated by the cross-bridge,
causes the muscle perimeter increase, which stresses the above-mentioned
muscle envelopes and then, after a short latency period, the muscle shortening process begins. The radial and longitudinal forces evoked by the crossbridges take part in it and are transmitted to the collagen helica, situated in
46
1. Bourne RB, Rorabeck CH. Compartment syndromes of the lower leg. Clin
Orthop 1989, 240: 97–104.
2. Fields RW. Mechanical properties of the frog sarcolemma. Biophysical J 1970:
462–479.
3. Gavronski G, Veraksits A, Vasar E, Maaroos J. Evaluation of viscoelastic
parameters of the skeletal muscles in junior triathletes. Physiol Meas
���������������
2007, 28:
625–637.
4. Jerosch J. Intrafasciale Druckmessungen in der Tibialis anterior – Lage in
Abhangigkeit von Korperlage und Gelenkstellungen. Biomed
�����������������������
Techn 1989, 34:
9, 202–206.
5. Järvholm V, Palmerud G, Herberts P, Hogfors C, Kadefor R. Intramus­
cu­lar pressure and electromyography in the supra����������������������������
spinatus muscle at shoulder
abduction. Clin Ortop 1989,
�������������������
245: 102–109.
�������������
6. Kirby RL, Marlow RW, MacLeod DA, Marble AE. The effect of locomotion speed on the anterior tibial intramuscular pressure of normal humans.
J Biomechanics 1988, 21 (5): 357–360.
7. Korhonen RK, Vain A, Vanninen E, Viir R, Jurvelin JS. Can mechanical
myotonometry or electromyography be used for the prediction of intramuscular
pressure? Physiol Meas 2005, 26: 951–963.
47
Acta Academiae Olympiquae Estoniae Vol. 14 No. 1/2, pp 49–68, 2006
8. Maughan DW, Godt RE. Radial forces within muscle fibers in rigor. J Gen
Physiol 1981, 77 (1): 49–64.
9. Monti RJ, Roy RR, Hodgson JA, Edgerton VR. Transmission of forces within mammalian skeletal muscles. Journal of Biomechanics 32, 1999: 371–380.
10. Patel TJ, Lieber RL. Force Transmission in Skeletal Muscle: from Actomyosin
to External Tendons. In: Exercise and Sport Sciences Reviews. Baltimore,
Philadelphia, Hong Kong, London, Munich, Sydney, Tokyo: Williams &
Wilkins 1997, 25: 321–363.
11. Street SF, Ramsey RW. Sarcolemma: transmitter of active tension in frog skeletal muscle. Science 1965, 149: 1379–1380.
12. Vain A. On the Phenomenon of Mechanical Stress Transmission in Skeletal
Muscles. Tartu: Tartu University Press 1990.
13. Vain A. A New Biomechanical Model of the Skeletal Muscle. In: Abstracts
Second World Congress of Biomechanics. Amsterdam: 1994, I: 87.
14. Vain A, Kaljuvee A. Dependence of the Force Evoked in the Collagen Helix
of Muscle Fibre on the Length of Sarcomere in Contraction and Streching. In:
Book of Abstracts XVIth Congress of the International Society of Biomechanics.
University of Tokyo 1997, 245.
15. Vain A. Method and Device for Recording Mechanical Oscillations in Soft
Biological Tissues. US Patent No. 6132385, 2000.
16. Vain A, Viir R. A New Diagnostic Technique for Peripheral Spinal Muscle
Stiffness Measurements. In: Brock M., Schwartz W., Wille C., eds. First
Interdisciplinary World Congress on Spinal Surgery and Related Disciplines.
Berlin: Monduzzi Editore 2000, 807–811.
48
INFLUENCE OF TRIGENICS MYONEURAL
TREATMENT ON LOWER EXTREMITIES’ MUSCLE
TONE AND VISCOUS-ELASTIC PROPERTIES IN
YOUNG BASKETBALL PLAYERS
M. Vahimets1,2, H. Gapeyeva1,2, J. Ereline1,2, M. Pääsuke1,2,
P. Kaasik1, A. Vain3
Institute of Exercise Biology and Physiotherapy,
Estonian Centre of Behavioural and Health Sciences,
3
Institute of Experimental Physics and Technology,
University of Tartu, Tartu, Estonia
1
2
Abstract
The training load in basketball has sharply increased, imposing bigger demands on the neuromuscular system of athletes. �����������������������
A structured programme
of warm-up exercises can prevent knee and ankle injuries in young people
practising sports. Trigenics
��������������������������������������������������
Myoneural Treatment (TMT) combined with
Eastern manual medicine and modern neurophysiology is based upon a neurological rather than mechanical model of treatment. The procedures involve synergistic, simultaneous application of three treatment techniques that
strongly facilitate neurological pathways involved with muscle relaxation
and pain reduction – neurogenics (reflex neurology), myogenics (mechanoreceptors manipulation), autogenics (biofeedback). One of the possibilities for influencing athletes’ skeletal muscles and increase neuromuscular
efficiency is the application of Trigenics treatment system. The aim of the
present study was to estimate the influence of Trigenics treatment system
on lower extremities muscles tone and viscous-elastic properties in young
basketball players.
Six young male basketball players of Estonian national team aged 15.3 ±
0.5 (mean ± SE) year (BMI 21.7 ± 2.3) participated in the study.������������
Their �����
training load was 6 h per week and duration of sports training 7.0 ± 1.7 years.
Six TMT procedures were performed twice per week on training-free days.
49
The tone (characterized by frequency of muscle oscillation at rest) elasticity
(characterized by logarithmic decrement of oscillations’ damping) and stiffness of lower extremities’ muscles (m. tibialis anterior, m. gastrocnemius
c. meiale, m. rectus femoris, m. biceps femoris c. longum) were evaluated
bilaterally using myometer Myoton-3 (MultiScan mode, 20 measurements
in each area) and software Myoton elaborated at the University of Tartu. The
method of myometry is based on dosed impact on muscle belly, after which
a muscle as viscous-elastic structure replies with damped oscillation. The
areas for measurements (the middle part of muscle belly) were identified by
manual palpation at muscle contraction. Tone characteristics were estimated
at rest before first and after six TMT procedures.
After the application of TMT procedures the significant change (p
�����
<
0.05) ����������������������������������������������������������������������
of muscle tone, elasticity and stiffness was found in the majority of
subjects for above listed muscles. Significant decrease of tone and stiffness
(p < 0.05) ���
of m. gastrocnemius was found as compared with data before
procedures extending over 21% in some subjects. Greater improvement �����
(p <
0.05) of
������������������
elasticity for m. gastrocnemius was noted in athlete 3 (33 and 13%
for right and left leg, respectively). Significant decrease of muscle stiffness
was found in the majority of subjects for studied muscles.
Keywords: myometry, elasticity, stiffness, athletes
Introduction
The musculoskeletal system enables us to act out and express our human
existence and it is the greatest energy user in the body, as well as one of our
primary sources of pain, discomfort and disability, whether localized or general, referred or reflex, acute or chronic. For the purpose of accuracy, a comprehensive term can be used to describe all lesions of the musculoskeletal system
– osseous and soft tissue – and this term is somatic dysfunction [4].
The central nervous system (CNS) plays significant role in optimizing the
selection of muscle synergies to produce movement [14]. Muscles work as
force couples to produce force, dynamically stabilize, and reduce force efficiently. The CNS recruits the appropriate muscles in a synergy during speci-
50
fic movement patterns [8]. Optimum posture enables the development of
high levels of muscle strength and neuromuscular efficiency. Muscle strength
permits the neuromuscular system to perform dynamic, eccentric, isometric
and concentric actions in a multi-planer environment [10]. Neuromuscular
efficiency is the ability of the neuromuscular system to allow agonists, antagonists and synergists to work together to reduce force, stabilize and produce
force efficiently [10]. When the muscular, articular and neural systems are
activated during functional movements, the cumulative information from all
structures is sorted out by the CNS (sensorimotor integration) [7].
The training loads in basketball have sharply increased, imposing bigger demands on the neuromuscular system of athletes. High training loads
influence the joints, muscles, ligaments, tendons, and can be followed by
the elasticity and the tension of muscles being decreased, thus increasing
the danger of injury. A structured programme of warm-up exercises can prevent knee and ankle injuries in young people practising sports. Preventive
training should therefore be introduced as an integral part of youth sports
programmes [15]. If the muscles are shortened or lengthened beyond the
optimum length, the amount of tension that the muscle is able to generate
decreases [18]. Trigenics Myoneural Treatment (TMT) system combined
by Eastern manual medicine and modern neurophysiology is based upon a
neurological rather than mechanical model of treatment and is��������������
applied in a
similar manner to the work of Travell and Simons [20]. The principles of
reciprocal inhibition [18] are applied to allow deeper access into the muscle with reduced pain and resistance. Using the inverse myotatic reflex [8],
muscles are then lengthened to re-establish healthy neuromusculoskeletal
dynamics and prevent further injuries.
The procedures involve synergistic, simultaneous application of three
treatment techniques that strongly facilitate neurological pathways involved
with muscle relaxation and pain reduction – neurogenics (reflex neurology),
myogenics (mechanoreceptors manipulation), autogenics (biofeedback). One
of the possibilities is to influence sportsmen’s skeletal muscles and increase
neuromuscular efficiency using TMT.
The aim of the present study was to estimate the influence of TMT procedures on lower extremities muscles tone and viscous-elastic properties in
young basketball players.�
51
Methods
Subjects. Six young male basketball players of the Estonian national team
(U-16) aged (mean ± SE) 15.3 ± 0.5 years with BMI 21.7 ± 2.3 kg·m-2 participated in the study.������������������������������������������������������
Their training
�����������������������������������������������
load was 6 h per week and duration of
sports training 7.0 ± 1.7 years. ����������������������������������������
Six TMT procedures were performed twice
per week on training-free days. The
��������������������������������������������
tone and elasticity of muscles of lower
extremity (m. tibialis anterior, m. gastrocnemius c. mediale, m. rectus femoris, m. biceps femoris c. longum) were evaluated at rest bilaterally by
Myoton-3 and software Myoton.
Myometry. Myometer Myoton and the method of myometry were elaborated at the University of Tartu by A. Vain in 1979 [21, 23, 25]. The working
principle of the device is based on the dosed impact on muscle belly, after
which muscle as viscous-elastic structure replies with damped oscillation.
The muscle tone is characterized by frequency of muscle oscillation [Hz]
at rest ��������������������������������������������������������������������������
(or at relaxation)��������������������������������������������������������
. The muscle elasticity, i.e.
�������������������������������
the ability of the muscle
to restore its initial shape after contraction, is �����������������������������
characterized by logarithmic
decrement of oscillations’ amplitude damping [22, 24]. Stiffness of muscle
characterizes the ability of tissue to restore its shape after removing of external force acting on muscle. T������������������������������������������������
he mass of the testing end of Myoton-3
������������������
(Fig.
���������
1)
is 20 g and the kick time of testing end during all measurements was 15 ms.
Four muscles of lower extremities were tested bilaterally: foot dorsal
flexor (m. tibialis anterior), foot plantar flexor (m. gastrocnemius c. mediale), knee flexor (m. biceps femoris c. longum), knee extensor (m. rectus
femoris).
The muscle tone characteristics were evaluated at rest using MultiScan
mode of myometer performing 20 measurements in each area before the first
and after six TMT procedures.�����������������������������������������������
����������������������������������������������
The area for measurements (the middle part of
muscle belly) was identified by manual palpation at muscle contraction [9].
The testing end of myometer was placed on previously palpated muscle belly.
The points for measurements were marked symmetrically for muscles of right
and left body side. While registering the tone characteristics of foot dorsal
flexor and knee extensor muscles, the subject was in supine position; in case
of foot plantar flexor and knee flexor muscles measurements the subject was
in prone position (Fig. 2). Data were analysed using software ��������
Myoton��.
52
Figure 1. Myoton-3 – device for the measurement of muscle tone, elasticity
and stiffness.
Figure 2. Testing of muscle tone and viscous elastic properties of lower
extremity muscles using Myoton-3; A – m. tibialis anterior, B – m.
gastrocnemius c. mediale, C – m. rectus femoris, D – m. biceps femoris
c. longum.
53
Trigenics Myoneural Medicine. An appealing aspect of Trigenics is
that it functions also as active resistance exercise, involving direct therapeutic interaction between the patient and the registered Trigenics practitioner (instructor).��������������������������������������������������������
The three main components used in Trigenics facilitate
neurological pathways involved with muscle relaxation and pain reduction
while localized pressure is applied to the TMT: ������������������������
neurogenics (reflex neurology), myogenics (mechanoreceptor manipulation), autogenics (biofeedback). In the present work the following TMT ����������������������������
procedures have been used:
muscle test, strengthening and lengthening procedures. Muscle tests were
performed before procedures [9].
����
M. tibialis anterior. Muscle test: patient is in supine position, knee extended,
with foot resting off the end of the table. The foot is dorsiflexed and inverted.
Pressure is applied by the instructor on the involved foot from the medial/superior side, the patient attempting to evert and plantarflex the foot [9].
Strengthening procedure: patient is in supine position. The legs are extended along the table with the feet hanging off the end of the table. Instruc­
tor stands near the foot facing cephalad (Fig. 3A, B). The furthest hand from
the involved side makes a thumb contact on the muscle, supporting hand
supports the involved foot by placing the hand on the plantar surface and
is positioned to resist ankle plantarflexion. The patient will first evert, then
fully plantarflex the foot. The instructor will lightly resist this movement,
yet allowing full range of motion.
Lengthening procedure: patient is in supine position, legs are in the same
position ������������������������������������������������������������������
(Fig. 3C, D).�����������������������������������������������������
����������������������������������������������������
Instructor������������������������������������������
stands in the same way as in case of the
strengthening procedure, supporting hand is placed on the dorsum of the
foot, across the metatarsals and brings the foot into plantarflexion and eversion to begin the procedure. The patient will attempt to dorsiflex and invert
the foot and �����������������������������������������������������������������
instructor�������������������������������������������������������
will resist this movement, allowing for minimal range
of motion.
M. gastrocnemius caput mediale. Muscle test: the involved leg is flexed
at the knee by 110° with the foot resting on the table. The lower leg is internally rotated to test the medial head of the muscle. ��������������������������
Instructor����������������
is standing on
the involved side, the furthest hand is placed on the knee to stabilize it, the
other hand cups the calcaneus on the involved side. Pressure is applied with
this hand to extend the knee along the horizontal plane of the table.
54
Figure 3. Strengthening (A – start, B – finish) and lengthening (C – start,
D – finish) TMT procedures for m. tibialis anterior.
Strengthening procedure: patient is in prone position, knee flexed by 90°
(Fig. 4A, B).������������������������������������������������������������������
Instructor
�����������������������������������������������������������������
is����������������������������������������������������
standing at the foot of the table, the nearest arm
reaches under and around the patient’s foot and ankle, so that the dorsum
of the foot rests against the forearm. The patient dorsiflexes and inverts the
ankle while lightly extending the knee allowing the patient to extend the
knee to a relatively small degree.
Lengthening procedure: patient is in prone position, knee fully extended,
the foot resting off the end of the table ��������������������������������������
(Fig. 4C, D).�������������������������
Instructor��������������
������������������������
supports the
patient’s foot so that the plantar aspect of the foot is resting against the distal
thigh of the �����������������������������������������������������������������
instructor�������������������������������������������������������
. The patient attempts to plantarflex the ankle by pushing against the i�����������������������������������������������������������
nstructor��������������������������������������������������
’s supporting leg, contracting the muscle approximately for 5–6 seconds. Instructor��������������������������������
������������������������������������������
allows minimum range of motion.
55
placed against the shin and brings the knee of the involved side into maximum flexion, instructor wrapping the fingers of both hands (if possible) under the involved leg. The forearm of the proximal arm can be used to hold
down the pelvis. The hand that is most distal is also used as a supporting
hand, lifting the knee off the table to extend the involved hip. The patient
attempts to flex the involved hip by pushing the knee towards the table.
Simultaneously, patient is also asked to extend the involved leg by pressing
the foot and lower leg against instructor������������
����������������������
’s shoulder.
Figure 4. Strengthening (A – start, B – finish) and lengthening (C – start,
D – finish) TMT procedures for m. gastrocnemius.
M. rectus femoris. Muscle test: patient is in supine position, leg is flexed at
the hip by 30°, lower leg is in neutral position or internally rotated by approximately 45°. Instructor��������������������������������������������������
������������������������������������������������������������
is standing on the uninvolved side, the cephalad
hand supports the anterior aspect of the ilium, the other hand is placed on the
anterior aspect of the patient’s distal tibia. Pressure is applied with this hand
straight down, in the sagittal plane.
Strengthening procedure: patient is in supine position (Fig.
������������������
5A, B).�����
The
hip and knee on the involved leg are flexed. Instructor��������������������
������������������������������
is standing on the
involved side of patient, the hand nearest to the table is placed on the knee
of the involved leg. I���������������������������������������������������������
nstructor������������������������������������������������
maximally flexes the patient’s hip by bringing
the knee up towards the chest with the supporting hand.�
Lengthening procedure: patient is in prone position, lying on the involved side of the table, uninvolved leg is hanging off the side of the table ������
(Fig.
5C, D).�����������������������������������������������������������������������
The uninvolved leg is fully flexed and patient is trying to place the
foot flat on the floor. The involved leg is flexed at the knee by 90°. Instructor
�����������
is��������������������������������������������������������������������������������
standing on either side of the patient. The shoulder closest to the patient is
56
Figure 5. Strengthening (A – start, B – finish) and lengthening (C – start,
D – finish) TMT procedures for m. rectus femoris.
M. biceps femoris c. longum. Muscle test: patient is in supine position. The
involved leg is flexed at the knee approximately 100° and the tibia of the
involved leg is externally rotated. Instructor��������������������������������
������������������������������������������
is standing at the foot of the
table, facing cephalad. The furthest hand from patient is placed on the knee
of the involved leg to stabilize it, the other hand cups the calcaneus passing
under the foot. Pressure is applied with this hand to extend the knee, along
the horizontal plane of the table.
57
Strengthening procedure: patient is in prone position, the knee of the involved side is flexed by about 110° (Fig.
��������������������������������������������
6A, B).�������������������������������
������������������������������
Instructor��������������������
is standing on the
involved side, caudal hand is used to support the involved leg on the dorsum
of the foot and ankle. Patient’s leg is brought into flexion with some external
rotation as a starting position. The patient is asked to extend and slightly
internally rotate the leg by moving the foot down and in toward the floor.
Lengthening procedure: patient is in prone position, the hip is maximally
flexed and the knee is slightly bent ��������������������������������������������
(Fig. 6C, D).�������������������������������
������������������������������
Instructor��������������������
is standing on the
involved side with the calf or ankle of patient’s foot placed on the shoulder
of instructor���������������������������������������������������������������
�������������������������������������������������������������������������
. Patient attempts to extend the hip by pushing the entire leg
forward. During the contraction, the knee will also extend fully. Following
the contraction phase, the ����������������������������������������������������
instructor������������������������������������������
brings the involved leg into further flexion.
Figure 6. Strengthening (A – start, B – finish) and lengthening (C – start,
D – finish) TMT procedures for m. biceps femoris.
All TMT procedures for four muscles were performed initially on the right
and then on the left body side. The duration of TMT procedures for one
athlete was 15 minutes.
58
Statistics. Data are mean and SD. Data were analysed using Myoton
(mean and SD) and MS Excel XP software. Changes of data after TMT procedures were calculated in percentage, where characteristics of tone, elasti­
city and stiffness before the first procedure were accepted as 100%. The
����
level of p < 0.05 was selected to indicate statistical significance.
Results
Different individual changes of muscle tone, elasticity and stiffness of lower
extremity muscles were established for right and left body side in young
basketball players, using the myometer. Both legs of the studied 6 athletes
were tested before the 1st and following six TMT procedures (total of 12
legs).
Changes of muscle tone after six TMT procedures are shown on Fig. 7.
Significant increase (p < 0.05) of muscle tone of m. rectus femoris (Fig. 7A)
was noted for 3 legs (athlete 1, 4 and 6) and decrease (p < 0.05) also for 3
legs (athlete 3, 4 and 6). For two athletes the effect of TMT procedures differed on the muscles of right and left side (athlete 4 and 6). Greater decrease
of tone was found in the athlete 4 and 6 (by 10 and 11%, respectively), and
increase in athlete 6 (17%).
Significant increase (p
��������������������������
< 0.05) ���������������
of the tone of m. biceps femoris (Fig. 7B)
was observed for 4 legs (in athlete 3 for both legs; athlete 4 and 6) and
increase (p
���������������������������������������������������������������������
< 0.05) for
����������������������������������������������������������
2 legs of the athlete 5. Greater decrease of tone was
noted in athlete 5 (9%) and increase in athlete 3 (12%).
Following the application of six TMT procedures, the significant de­
crease (p
��������������������������������������������������������������������
< 0.05) ���������������������������������������������������������
of muscle tone was found in the majority of subjects for
m. gastrocnemius (for 6 legs) (������������������������������������������
Fig. 7C)����������������������������������
. Significant decrease (p
�����������
< 0.05)
of the tone of m. gastrocnemius was found as compared with data before
procedures – e.g., for right leg it was 19% in athlete 4 and 33% in athlete 3.
In two athletes decrease of tone was significant for both legs (athlete 2 and
4). Greater increase of tone was noted in athlete 6 (18%).
After six TMT procedures the tone of m. tibialis anterior significantly
decreased (p
��������������������������������������������������������������������
< 0.05) for
���������������������������������������������������������
3 legs (athlete 1, 4 and 6) and increased �����������
(p < 0.05)
59
for 3 legs (athlete 4, 5 and 6) (Fig.
�����������������������������������������������
7D)��������������������������������������
. Greater decrease of tone was in the
athlete 6 (7%) and increase in athlete 5 (11%).
was observed in one athlete (6, 26%) (Fig. 8A). Significant increase (p <
0.05) of decrement (worsening of elasticity) for m. rectus femoris was noted
in 4 legs (athlete 2 and 3), maximal increase 21% (in athlete 2).
Significant decrease (p < 0.05)������������������
of
�����������������
decrement for m. biceps femoris was noted�
for 5 legs (in athlete 4 for both legs; athlete 1, 5 and 6) and s�����������������������
ignificant increase (p
< 0.05) for 3 legs (in athlete 2 for both legs; athlete 5) (Fig. 8B). �����������������
Greater increase
of decrement was noted in athlete 2 (30%) and decrease in athlete 4 (30%).
Significant decrease (p
����������������������������
< 0.05) of
�����������������
decrement for m. gastrocnemius was
noted in 2 legs (athlete 3) and increase ���������������������������������������
(p < 0.05) ����������������������������
in 4 legs (athlete 1, 4 and
6) (Fig.
��������������������������������������������������������������������������
8C)�����������������������������������������������������������������
. Greater increase of decrement was noted in athlete 4 (33%) and
decrease in the athlete 3 (31%). Changes in elasticity were greater in athlete 3
for m. gastrocnemius (improving 33% and 13% for right and left leg, respectively).
Significant decrease ����������������������������
(p < 0.05) �����������������
of decrement for m. tibialis anterior was
noted in 3 legs (left leg of athlete 1, 4 and 6) and increase (p
����������������
< 0.05) in
�����
3
legs (for both legs of athlete 2 and left leg of the athlete 5) (Fig.
�������������������
8D).���������
Greater
increase of decrement emerged in athlete 2 and 6 (20%, and in athlete 2 it
was noted for both legs). Decrease in this parameter was found in athlete 4
(23%).
Figure 7. Tone of lower extremities’ muscles (characterized by frequency of
muscle oscillation at rest [Hz]). A – m. rectus femoris, B – m. biceps femoris
caput longum, C – m. gastrocnemius caput mediale, D – m. tibialis anterior.
Changes of elasticity of muscles after six TMT procedures are shown on
Fig. 8. Decrease (p < 0.05) of decrement (improving of elasticity of muscle)
60
61
Changes of stiffness of muscles after six TMT procedures are shown on Fig. 9.
After application of six TMT procedures the significant decrease of muscle
stiffness was found in the majority of subjects for studied muscles.
Figure 8. Elasticity of lower extremities’ muscles (characterized by
logarithmic decrement of oscillations’ amplitude damping). A – m. rectus
femoris, B – m. biceps femoris caput longum, C – m. gastrocnemius caput
mediale, D – m. tibialis anterior.
62
Figure 9. Stiffness of lower extremities’ muscles. A – m. rectus femoris, B – m.
biceps femoris caput longum, C – m. gastrocnemius caput mediale, D – m.
tibialis anterior.
63
Significant decrease ��������������������������������������
(p < 0.05) ���������������������������
of stiffness was noted for m. rectus femoris in
5 legs (in athlete 3 for both legs; athlete 2, 4 and 5) and increase �����������
(p < 0.05)
in 3 legs (athlete ������������������������������������������������������������
1�����������������������������������������������������������
, 4 and 6) (Fig. 9A). Greater
�������������������������������������
decrease occurred in athlete
4 (9%) and increase in athlete 6 (19%).
Significant decrease (p
����������������������������
< 0.05) of
�����������������
stiffness for m. biceps femoris was
observed in 3 legs (athletes 3–5) and increase (p
��������������������������������
< 0.05) ���������������������
in 2 legs (athlete 2
and 3) (Fig.
���������������������������������������������������������������������
9B).�����������������������������������������������������������
Greater decrease was found in athlete 4 (6%) and increase
in athlete 2 (5%).
Significant decrease (p
����������������������������
< 0.05) �����������������
of stiffness for m. gastrocnemius was
found in all studied legs of all athletes (except of left leg of 6th subject)
(Fig. 9C)�����������������������������������������������������������������
. Greater decrease was found in athlete 4 (15% and 14% for right
and left leg, respectively).
Stiffness of m. tibialis anterior decreased significantly (p
����������������
< 0.05) in 7
legs (athlete 1, athletes 3–6) and increased (p < 0.05) in one leg (left leg of
athlete 2) after six TMP procedures (Fig. 9D). Greater
������������������������������
decrease of stiffness
was noted in athlete 4 (16% for right leg) and increase in athlete 6 (4%).
Discussion
The subjects of the present study were young basketball players at the age
of 15. Proper development of muscles is crucial for daily musculoskeletal
stability and any athlete’s performance, particularly those who participate in
power sports. Basketball is definitely one of them.
This study demonstrated that the majority of subjects had significantly
higher tone of muscles before TMT procedures than after them. The reason for
this may be inadequate or insufficient muscle care. After six procedures the tone
and stiffness of muscles decreased in some cases by 33% (athlete 3). TMT is
for athletes a good alternative with a considerable potential, accelerating the
rehabilitation process. Any kind of muscle manipulation is beneficial for
young athletes’ muscle care.
From TMT point of view, it is important for any athlete to possess structural efficiency. Studies by Shambaugh et al. [17], Power et al. [16], Watson
[27], and Cowan [6] indicated that deficiencies in posture are important
64
predictors of specific types of sport injury. Watson [27] noted that posture
evaluation must be quantitative, precise and carefully carried out if it is to
be of value in the prediction of sport injury. Furthermore, the athlete must
also possess functional efficiency, which permits the neuromuscular system
to perform functional tasks with the least amount of energy and will create
the least amount of stress on the kinetic chain.
Many authors have demonstrated significant correlation between the biomechanical characteristics and the working capacity of CNS [1, 26]. The
biomechanical characteristics play a great role in elastic deformations and
energy recuperation processes because the muscles are stretched out prior
to entering their basic phases [3, 12]. The
����������������������������������
energy recuperation mechanism
of elastic deformations is the most effective. It has been shown in track and
field events like running, jumps and throws [2, 11].
Prevention and intervention of injury have become focal points for researchers and clinicians. Before these studies can be used, the risk factors
for injury must be clearly established [28]. Many injury risk factors, both
extrinsic (those outside of the body) and intrinsic (those from within the
body), have been suggested [19, 28]. Extrinsic risk factors include the level
of competition, skill level, shoe type, use of ankle tape or brace and playing surface. Intrinsic risk factors include age, sex, previous injury and inadequate rehabilitation, aerobic fitness, body size, limb dominance, flexibility,
limb girth, muscle strength, imbalance and reaction time, postural stability,
anatomical alignment, and foot morphology.
Messina et al. [14] found a greater number of injuries occurring during
games than in the training period in a prospective study of 1863 male and female high school basketball athletes. A reportable injury was one that resulted
in any time loss from participation, an incident that necessitated a consultation
with a doctor, or one that involved the head or face. The ankle and knee were
the most commonly injured body parts in both boys and girls.
In the present study, the changes of elasticity were observed in athletes
after six TMT procedures. Decrement
������������������������������������������������
characterizes muscle elasticity, i.e.
the ability of the muscle to restore its initial shape after contraction. The
lower the decrement, the better are the elasticity of muscle and the ability
of contraction. This study indicated improvement of muscle elasticity in the
65
majority of subjects, but not in all cases. The individual choice of the duration and techniques of manipulations must be applied for athletes’ muscle
care to attain maximal positive effect.
Of sports injury cases recorded at Iowa Junior Olympics in 1985, 34%
required attention only from coaches, 46% were referred to local physicians, and 20% were referred to specialists [13]. This study found that out
of patients who sought Western medical help, 17% required treatment from
orthopaedic surgeons to correct or treat outstanding injury and 74.6% were
treated by orthopaedic doctors or physical therapists. More than half of patients sought treatment from Eastern medicine, including traditional massage
(64%), acupuncture (58%), and Chinese treatment applications (65%).
The completely different medical approaches of the Eastern and Western
medicine are widely accepted by elite athletes and coaches. Mainstream
Western medicine doctors should not overlook the traditional Eastern medicine, and they should learn more about these alternative treatment met­hods
and apply them effectively. If Western doctors can work together with
Eastern traditional doctors, we can improve our medical network [5].
Conclusions
After six Trigenics Myoneural Treatment procedures significant decrease of tone and stiffness of m. gastrocnemius was noted in the majority of
young basketball players as compared to the pre-therapy condition. Thus
the improvement of the functional condition of muscular tissue occurred.
The measurement of muscle tone characteristics is an additional tool for
the observation of neuromuscular system condition of athletes and for the
individualisation of procedures for increasing their effect.
References
1.Aruin AS, Zatsiorski VN����������������������
, Panov G, Raitsin AM. Equivalent biomechanical
characteristics of ankle joint muscles. Fisiologia cheloveka, 1978, 4 (6): 1072–
1079. (Аруин АС, Зациорский ВН, Панов Г, Райцин АМ. Эквивалентные
66
биомеханические характеристики мышц голеностопного сустава.
Физиология человека, 1978, 4 (6): 1072–1079 (in Russian).
2. Asmussen E, Bonde-Petersen F. Storage of elastic energy in skeletal muscles
in man. Acta Physiol Scand, 1974, 91: 385–392.
3.Cavagna GA, Dusman B, Margaria R. Positive work done by previously
stretched muscle. J Appl Physiol, 1968, 24: 21–32.
4.Chaitow L. Modern Neuromuscular Techniques. Churchill Livingstone. 2nd
ed: 2003, 1–6.
5.Chen SK, Cheng JM, Lin JC, Hong YJ, Huang PJ, Chou PH. Investigation
of management models in elite athlete injuries. Kaohsiung J Med Sci, 2005, 21
���
(�������������
5): 220–227.
6. Cowan DN, Jones BH, Frykman PN, Polly DW Jr, Harman EA, Rosenstein
RM, Rosenstein MT. Lower limb morphology and risk of overuse injury
among male infantry trainees. Med Sci Sports Exerc, 1996, 28 (8): 945–952.
7. Enoka R. The Neuromechanical Basis of Kinesiology; Human Kinetics
Publishers 1988, 138–141.
8.Ikai T. et al. Reciprocal Inhibition in the Forearm During Voluntary Contraction
and Thinking About Movement. Electromyogr Clin Neurophys, 36 (5): JulyAugust, 1996: 295–304.
9. Kendall FP, Kendall McCreary E, Provance PG. Muscles: Testing and
Function: with Posture and Pain. 4th ed. Philadelphia etc. Lippincott Williams
& Wilkins, 1993.
10. Knott M, Voss DE. Proprioceptive Neuromuscular Facilitation: Patterns and
Techniques, 2nd ed.: New York: Hoeber Medical Division, Harper and Row,
1968.
11. Komi PV, Bosco C. Utilization of stored elastic energy in leg extension muscles by men and women. Med Sci Sports, 1978, 10 (4): 261–265.
12. Levin A, Wyman J. The viscous-elastic properties of muscle. Proc Poy Soc B
(London), 1927, 101: 218–243.
13.Martin RK, Yesalis CE, Foster D, Albright JP. Sport injuries at 1985 Junior
Olympics. An epidemiologic analysis. Am J Sport Med, 1987, 15: 603–608.
14.Messina DF, Farney WC, DeLee JC. The incidence of injury in Texas high
school basketball. A prospective study among male and female athletes. Am J
Sports Med, 1999, 27: 294–299.
15.Olsen OE, Myclebust E, Engebretsen L, Holme I, Bahr R. Exercises to
Prevent Lower Limb Injuries in Youth Sports: Cluster Randomised Control
Trial. BMJ, 2005, 26: 330 (7489): 449.
16.Power CM, Mafucci R, Hampton S. Rearfoot posture in subjects with patellofemoral pain. J Orth Sports Phys Ther, 1995, 22:155–160.
67
17. Shambaugh JP, Klein A, Herbert JH. Structural measures as predictors of
injury in basketball players. Med Sci Sports Exercise, 1991, 23: 522–527.
18. Sherington CS. Reciprocal innervation of antagonist muscles. Fourteenth note.
On double reciprocal innervation. Proc R So Lond B Biol Sci, 91: 1909, 249–
268.
19. Taimela S, Kujala UM, Osterman K. Intrinsic risk factors and athletic injuries. Sports Med 1990, 9: 205–215.
20.Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point
Manual. Williams and Wilkins, Baltimore, 1998.
21. Vain A. The damped oscillation method for diagnostics of functional state of
human skeletal muscles. In: Methods of Vibrational Diagnostics of Rheological
Properties of Soft Materials of Biological Tissue. Gorki, 1979, p. 116–125
(��������������
Вайн А. Метод �����������������������������������
затухающих колебаний в диагностике ����������������
функционального
состояния скелетных мышц человека. В сб. Методы вибрационной диагностики реологических свойств мягких материалов биологических тканей. Горький, 1979, стр. 116–125.) (in Russian).
22. Vain A. On the tone of the skeletal muscle. Acta et Commentationes Univ.
Tartuensis. 1993, 958: 138–153.
23. Vain A. Estimation of the functional state of skeletal muscle. In: Veltink PH
& Boom HBK (Eds) Control of Ambulation using Functional Neuromuscular
Stimulation. Enschede: University of Twente Press, 1995, 51–55.
24. Vain A. Estimation of skeletal muscle elasticity on subtonic tension level. In:
Proceedings of the Estonian Academy of Sciences. 1999, 4, 312–321.
25. Vain A. Method and Device for Recording Mechanical Oscillations in Soft
Biological Tissues. US Patent 6132285, 2000.
26. Zimkin NV, Pahhomova TG. On relationship between stiffness, viscousity
and bioelectrical activity of human muscles. Fisiologicheskij zhurnal SSSR,
1972, 58 (7): 1099–1108. (��������������������
Зимкин НВ, Пахомова ТГ.
���� О
�� взаимосвязи
������������������
между
твердостью, вязкостью и биоэлектрической активностью мышц человека.
Физиологический журнал СССР, 1972, 58 (7): 1099–1108) (in Russian).
27. Watson AWS. Sport injuries related to flexibility, posture, acceleration, clinical
defects and previous injury in high level players of body contact. Sport. Int J
Sports Med, 2001, 22: 222–225.
28. Williams JGP. Aetiologic classification of sports injuries. Br J Sports Med
1971, 4: 228–30.
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CHRONICLES OF THE ESTONIAN
OLYMPIC ACADEMY
Acta academiae olympiquae Estoniae Vol. 14 No. 1/2, pp 70–77, 2006
46th International Session for
young participants
Darja Saar
Abstract
The International Olympic Academy (IOA) with its headquarters and educational centre in ancient Olympia, Greece, is the centre of Olympic education.
IOA has five basic educational programmes, as well as three additional specialized Olympic educational programmes for different key groups in sport.
One of the basic IOA Olympic education programmes includes the arranging of International Sessions for young participants. The two-week annual
session, traditionally held in June or July, is designed as an introduction to
Olympism and the Olympic movement. The IOA brings together a large
international group of young people who are primarily students, Olympic
athletes, people active in sport and teaching, or engaged in their respective
National Olympic Committees or National Olympic Academies.
The aim of the IOA is to educate, but more importantly, to motivate
young people to use the experience and knowledge gained during the session in promoting the Olympic ideals and educating others in their respective countries (www.ioa.org.gr).
Introduction
The 46th International Session for young participants took place in Olympia
from 19 June to 3 July, 2006. There were more than 220 participants, aged
from 20 to 35 years, representing 99 countries all over the world who could
attend 13 lectures during the session. Most of the lecturers were members
of the International Olympic Committee or well-known researchers in the
field of Olympism and sport. The main theme of the particular session was
Olympism, the narrower subject being sport and ethics. It is a specific feature of the IOA Sessions for young participants that they include lectures,
questions-and-answers sessions, group discussion meetings, reports presen70
ted by participants, field trips to archaeological sites and museums, and performing independent research in the library.
Lectures and questions-and-answers sessions
Heated discussions took place during the session and it was attempted to
reach common understanding and appropriative solutions for today’s issues
in the field of sport ethics.
The first lecture of the session was delivered by Mr Richard W. Pound
(Canada), member of the International Olympic Committee, Chairman of
the World Anti-Doping Agency on the subject “The fight against doping
in sport”. The report was focused on the structure of the doping-fighting
system in the world and measures to reduce the number of doping cases in
sport. The lecturer stressed the necessity of changing public attitude in the
related matter and placing more value on fair play and the fight against doping in sport. After each lecture the participants could ask questions to be
answered by the lecturer. The Estonian participants of this session stressed
that in addition to changing the public attitude, it is important to admit
public responsibility for doping in sport. For a long time sport has been
much more than the competition of amateur athletes. In sport countries
and their sport systems compete with each other. Athletes feel pressurized
by the National Olympic Committee, the national federation of the sport
event, sponsors and the government, so in order to achieve better results
and win medals they can be tempted to use doping. Better results in the
fight against doping in sport can be achieved by enforcing sanctions against national federations and Olympic committees rather than penalties to
single athletes. At present sport institutions are not motivated to contribute
to anti-doping activities.
The lecture of Dr Alexander Kitroeff (Greece), Professor in the
Department of History at Haverford College, USA “Fair play versus competing to win and Coubertin’s thought” was dedicated to the problems of
fair play in modern sport. The continuous increase in the role of business
practices, money and corporate sponsorship in sport sometimes unintentionally and at times inevitably creates a mentality among athletes and fans that
71
can be summed up as “winning at all costs”. This trend distorts the basic element of sport that can be described as sportsmanship or the spirit of fair play
[1]. The lecturer explained his perception of fair play definition, stressing
the importance of the principle of respect for the game. In the opinion of
Dr Kitroeff, a victory without honour, without the observance of fairness on
and off the field is antithetical to the purpose of sport (ibis). Today the majority of sport observers are pessimistic about promoting fair play principles
in sport and the success of fair play campaigns launched by the organizations of Olympic movement. The lecturer presented several examples of the
most infamous fair play violations in modern sport. Dr Kitroeff also gave an
overview about Coubertin’s understanding of fair play and the solution to
the particular problem. Coubertin suggested that the preserving of fair play
depended on acknowledging the idea of amateurism.
Dr Angela Schneider, Associate Professor at the University of Western
Ontario (Canada) provided the audience in her lecture “Fair play as
respect for the game” with an overview about fair play in sport, based on
the principles of respect for the game. She presented basic ideas of motivating athletes to respect the game, rules and traditions of sport and Olympic
movement. Dr Schneider highlighted the implications of viewing fair play
as respect for the game on two levels: the personal level of an individual
athlete, and the institutional level. On the personal level, the respect for
the game influences the action during the competition, attitude to the opponents, and one’s commitment to the game. The concept of fair play as
respect for the game also has implications for actions and decisions on the
level of policy [2]. It can be concluded that creating fair play values on the
individual level is not sufficient without creating the institutional structure
to support athletes’ respect for the game by making decisions which refer
to the best interests of the game concerned. Dr Schneider also shared her
experience of launching the Canadian programme “True Sport” for fair
play in sport promotion.
The lecture of Dr Kostas Georgadis, Associate Professor at the University
of Peloponnese, Dean of the International Olympic Academy (Greece) “The
Olympic education programme of the ATHOC 2004 and the Hellenic
Ministry of Education” dealt with the Olympic education programme for
young people and children that was implemented in Greece during 2000–2004
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in connexion with the Olympic and Paralympic Games of Athens in 2004. The
audience was provided with the programme back­ground, objectives and keygroup data, as well as the overview about similar educational programmes
conducted in the past and the basic concepts of Olympic pedagogy. The main
slogan of the Greek Olympic education programme in 2000–2004 “Be aware,
participate, learn, create” [3] pointed to the main aims of the project: providing
information about Olympic Games, promoting understanding of the ideals of
Olympism, enhancing the level of physical education in schools, strengthening the related contribution by volunteers. Participants of the session also got
information concerning the educational materials used in the programme and
the process of the programme implementation.
During the participants-lecturer discussion, the Estonian participants
stressed the necessity for educational programmes aimed at top-level athletes, coaches and officials, motivating their general awareness about the
Olympic movement and values of Olympic philosophy. The author of this
article presented to the audience some typical answers of athletes to the
question “What are the Olympic Games for you?” The answers were the
following: the opportunity to become famous, rich and get a high position in
the society. In the author’s opinion, the athletes who have answered in this
way are certainly far away from Coubertin’s Olympic movement values.
Mr Sylvain Paillette (France) delivered in his lecture “Looking for the
identity of the Paralympic movement” a report on the Paralympic movement activities in recent years, the related problems and plans. The lecturer
raised the issue of admitting the importance of the Paralympic movement
and inclusion of athletes with disabilities in sport. According to his opinion, the Olympic and Paralympic movements are still separate and serve
different aims, whereas the Olympic values seem to be more preserved in
the Paralympic movement than in the Olympic movement, because of the
commercialisation of the latter.
Mrs Laurel Brassey-Iversen (USA) in her lecture on the subject
“Programmes of Olympic education” shared with the audience her experience in educating children in the field of Olympism and giving practical
advice concerning the organization of school Olympic Games and different
educational activities. The lecturer stressed that conducting educational activities requires personal initiative and passion for promoting Olympic values, ra-
73
ther than extensive financial resources as could be imagined in the beginning.
Via educating children it is possible to enhance the awareness of their parents
as well about the Olympic movement and values of Olympism.
Dr Kostas Kartalis, Professor at the University of Athens (Greece) delivered in his lecture “Ethical and social values of the Olympic games”
a report on the organization of Olympic Games 2004 in Athens. The main
topic of the lecture was the philosophy and the main principles of infrastructure rebuilding and reorganization in Athens as the Olympic venue. During
the preparations for Olympic Games 2004, the Athens transportation system
was totally transformed and several new social objects like sport halls and
other facilities for public use emerged in the city. The most unpleasant thing
that the organizers of the Olympic games in Athens had to deal with was the
considerable increase of expenditures for ensuring the security of Games
participants after 11 September events in the USA.
The lecture of Mr Spyridon Maragkos (Greece) on the subject “The ath­
letes of the Olympic games – ‘captives’ to biological and moral factors”
was dedicated to the psychosomatic dependencies of athletes participating
in the Olympic games. The desire to win can have a negative influence on
athletes, causing physical dependency on the use of endogenous and exogenous substances as an adjustment of the nervous system to the expected result, as well as mental dependency as a behaviour syndrome, characterized
by compulsive and repetitive changes in the lifestyle.
Mrs Paquerette Girard-Zappelli, Special Representative of the Inter­
national Olympic Committee Ethics Commission (France) lectured on the
subject “The Ethics Commission and the Olympic movement”, providing the audience with the overview about the activity of the International
Olympic Committee Ethics Commission.
Dr Lamartine DaCosta, Professor at the Gama Filho University (Brazil)
showed in the lecture “Sport and poverty” the extent of work to be done
in including the poorest part of the society in sport. The lecturer highlighted
the importance of the inclusion process, since sport is first of all a tool for
improving the quality of social life. Sport is definitely related to the functioning of the society and cannot be treated solely as a sector of entertainment
economy.
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The lecture by Mr Sam Ramsamy, member of the International Olympic
Committee (South Africa) on the subject “Sport and ethics” provided the
audience with an overview about the basic ethical problems in modern sport.
There are numerous unanswered questions in this field, and it is important to
imbue the youth who are in need of decent role models, with the principles
of fair play and justice. We should teach youth to win with humility and
accept defeat with dignity, also encouraging the team spirit.
The lecture by Mrs Anita L. DeFrantz, Member of the International
Olympic Committee (USA) on the subject “Women in sport: gender equality and gender identity” was dedicated to the problems of the inclusion of
women in sport, especially the participation of females in sport as athletes
and officials.
The lecture by Mr Urs Lacotte, Director General of the International
Olympic Committee (Switzerland) on the subject “The Olympic movement” provided the audience with the survey of everyday activities, structure, and main principles of the International Olympic Committee.
Group discussions
All session participants were distributed into10 English-speaking and
2 French-speaking groups. Each group had 15–20 members, including 1–2
coordinators, secretary and reporters. All discussion groups got similar questions. In addition, groups were free to choose one optional issue or make up
their own question.
Cycle A
Question 1: What does Olympism mean to you? Do you think that the values
of Olympism could form the basis of pedagogy?
Question 2: Does doping contradict the ethical values of sport?
Question 3: What are the ethical dilemmas that athletes face today?
Question 4: What is the role of Olympic education?
Cycle B
Question 1: In the fight against poverty, what role could sport play?
Question 2: Can sport contribute to shaping ethical behaviour?
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Question 3: How could leaders (athlete, coach, official or administrator)
promote gender equity across all aspects of sport?
Question 4: What should be the relationship between the Paralympic movement and the Olympic movement?
Optional Questions
Question 1: Discuss the ethical and legal considerations which should govern the management of sport.
Question 2: Discuss ethics in the media – the role and duties of sports journalists.
Question 3: What is the Olympic ideal threatened by? Discuss the ways in
which the Olympic movement could deal with these threats.
Question 4: What is ethics and in what way is it related to sports?
References
1. Kitroeff A. “Fair Play” versus Competing to Win and Coubertin’s Thought, 46th
International Session for Young Participants, 2006.
2. Schneider A. Fair Play as Respect for the Game, 46th International Session for
Young Participants, 2006.
3. Georgiadis K. The Olympic Education Programme of the ATHOC 2004 and
of the Hellenic Ministry of Education, 46th International Session for Young
Participants, 2006.
Conclusions
We would like to sincerely thank the International and Estonian Olympic
Academies for the opportunity to attend the Session for Young Participants.
For young people who are interested in promoting Olympic movement and
sport, attending the session was a good chance to better understand the
Olympic movement values and the related topical problems, as well as participate in the process of finding solutions for them. The two weeks that
were spent in the company of high-ranking members of the International
Olympic Committee, sport researchers and Olympic movement enthusiasts
were most valuable. The participation in discussions, answering questions
and learning from the experience of others motivate you much more than
anything else for analyzing situations, finding concrete solutions and doing
one’s best in promoting Olympism and its values in one’s own country.
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77
INFORMATION FOR CONTRIBUTORS
The Acta Academiae Olympiquae Estoniae (AAOE) annual issue since
1993 has the aim to promote the philosophy of Olympism and the scientific
foundation for the Olympic movement. From the year 2002 two issues of the
AAOE per year are publicated.
Papers published in the AAOE may cover a wide range of topics on the
principles of Olympism, including, but not limited to:
• review papers on the training of Olympic athletes,
• sport philosophy, sociology, methodology and training,
• application of the principles of Olympism,
• history of Olympic Movement and sport,
• physical activity of children and adolescents.
Only original papers not publicised previously are acceptable for contribution. They are reviewed by the editors and, when appropriate, sent to outside
editorial consultants. The AAOE is referred to in the international database
of Sportdata.
Submit manuscripts in two copies and on a floppy disc to: Arved Vain,
Editorial Board, Acta Academiae Olympiquae Estoniae, Jakobi 5-112, 51014
Tartu, ESTONIA; e-mail addresses are: reele.remmelkoor@ut.ee and arved.
vain@ut.ee. Direct contact with editorial staff via arved.vain@ut. ee is
also recommended, one copy of the paper should be sent via e-mail to this
address, as this way technical problems demanding direct contact with the
authors can be solved in a more operative way. The deadlines for accepting
manuscripts for the next issues of the AAOE are May and October.
Manuscripts. Articles ordinarily may not exceed 10 printed pages. Manu­
scripts should be submitted in English, typewritten, double-spaced and with
broad margins. Articles should be divided into: abstract including 3–5 key
words, introduction, material and methods, results, discussion, acknowledgements (if any) and references.
ress, including postcodes, of the author responsible for correspondence and
offprints should be stated.
The Abstract page. The Abstract (not exceeding 150 words) is the summary of the paper.
References. The references should contain only authors cited in the
text, be numbered using Arabic numbers and listed on a special page in
alphabetical order. References must be written in the standard format
approved by the International Committee of Medical Journal Editors.
Citations in the text should refer to the number of the references, placed
in square brackets.
Example of references:
1. Journal article 2. Book chapter 3. Textbooks Tesch PA, Karlsson J. Muscle fiber types and
size in trained and untrained muscles of elite
athletes. J Appl Physiol 1985, 59: 1716–1720.
Sale DG. Neural adaptation to strength training.
In: Komi PV, ed. Strength and Power in Sports.
Blackwell, London, 1992, 249–265.
Åstrand PO, Rodahl K. Textbook of Work
Physiology, 3rd edn. New York: McGraw Hill,
1986.
Tables. Tables should be typed on separate sheets with self-explanatory heading.
Figures. The Figures are meant to clarify the text, but their number should
be kept to minimum. They must be identified with a label on the back, which
indicates the number, author’s name and the top. Details must be large
enough to retain clarity after size reduction. Figure legends must be typed
on a separate page at the end of the manuscript.
The title page of the manuscript should contain a concise informative title,
the authors’ full names, the names (in English) of departments and institutions to be attributed and their city of location. The name and postal add-
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