Michael Ro
Mon, Aug-12-02, 20:02
Dr. Wanona Wellspring, DN, wrote to a strength scientist:
<A lengthened muscle is a strengthened muscle.>
*** On the contrary, if stretching leads to a regular increase
in muscle length, then it may not be able to produce greater
force, since the process is one of optimisation, not
maximisation. The ability of a muscle to exhibit strength,
i.e. produce force, also depends on how its tendinous
attachment inserts into the bones comprising a given joint and
the positioning of that joint (and its neighbours) in space.
<The longer the anatomical length between the actin myosin
filiments the greater contractability of the muscle fibers.
Therefore, stretching and flexibility will gain more
strength.>
*** There is no "length" between the actin and myosin
filaments; they are juxtaposed alongside and among one
another, with the minute "heads" on the myosin filaments
forming cross bridges to active sites on neighbouring actin
filaments -- so, what do you mean by "the longer the
anatomical length between the actin myosin filiments (sic) the
greater contractability (sic) of the muscle fibers"? Also,
what do you mean by "stretching and flexibility will gain more
strength"? Stretching doesn't gain strength, nor does
flexibility, especially since flexibility is a synonym for
"Range of Movement" of a joint (not a muscle).
What Alexandre was referring to undoubtedly was research which
showed that the strength of certain muscles in birds was
increased by hanging loads on their wings for several days at
a time, not a few seconds or minutes of popular fitness class
stretches. While some of this work has been replicated in
animals, it has not been confirmed in humans yet.
However, some research into the acute effects of stretch on
strength production is noteworthy. For example, the rate of
decay of torque following stretch does not depend upon stretch
variables and the absence of significant changes in EMG
(electrical) activity suggests that reflex activity does not
account for the observed changes when large initial forces are
involved. Time-constants of decay are much greater than
time-constants of rise of isometric torque at the same muscle
length, indicating that interaction of series elastic
(connective tissue such as tendons) and contractile elements
is not the sole cause of prolonged torque following stretch.
Thus it seems that stretch temporarily enhances the intrinsic
contractile properties of human muscle, rather than the
nervous processes alone (Thomson & Chapman,
1988).
To examine the effects of strength training on "muscle", we
must remember that the muscle complex consists of both
contractile (actin-myosin) and non-contractile (collagenous
and elastic) components, so that what we are imposing on the
contractile components, we are also imposing on the n
on-contractile components. In this respect, animal studies
have produced the following findings regarding the effect of
exercise or inactivity on the connective or collagenous
tissues (see Chs 1 & 3 of Mel Siff's "Supertraining" for
greater detail about stretching science):
1989. Single exercise sessions and sprint training do not
produce significant increase in junction strength,
although sprinting produces marked increases in ligament
mass and in ratios of mass per unit length (Tipton et
al, 1967; Tipton et al, 1974). Hence, Tipton and
colleagues have concluded that junction strength changes
are intimately related to the type of exercise regime
and not solely to its duration.
1990. Regular endurance training can significantly increase
junction strength-to-bodymass ratios for ligaments and
tendons (Tipton et al, 1974; Tipton et al, 1975).
1991. Long-term endurance exercise programmes cause
significant increases in the junction strength of
repaired injured ligaments (Tipton et al,
1992). In this regard, Tipton et al (1975) suggested that an
increase in tissue capillarisation associated with
chronic exercise may enhance the availability of
endogenous hormones and stimulate blood flow to the
repairing tissue.
1993. Long-term training significantly increases the collagen
content of ligaments (Tipton et al, 1970).
1994. Ligaments become stronger and stiffer when subjected to
increased stress, and weaker and less stiff when the
stress is decreased (Tipton et al, 1970; Noyes, 1977).
1995. Ageing reveals changes in collagenous tissues similar to
those caused by immobilisation, with reduction in
strength and stiffness of ligaments occurring with
advancing age. These changes may be due not only to the
degenerative process, but also to reduced physical
activity, superimposed disease states and other
unidentified processes (Frankel & Nordin, 1980).
Studies of the mechanical and biochemical properties of
tendon reveal a close relationship between tensile strength
and the amount of collagen. Similarly, the concentration of
total collagen is higher for slow muscle than for fast
muscle. This difference also appears at the level of
individual muscle fibres, with the concentration of collagen
in slow twitch fibres being twice that in fast twitch fibres
(Kovanen et al, 1984).
For example, muscle endurance training increases the tensile
strength of both slow and fast muscles, as well as the
elasticity of the former (Kovanen et al, 1984). Other studies
have shown that prolonged running also increases the
concentration of collagen in tendon and the ultimate tensile
strength of tendon (Woo et al, 1981). This finding is relevant
to the limited prescription of off-season transitional or
general physical preparation (GPP) training.
In contrast with this finding, the concentration of collagen
in muscle is not altered by endurance training. However, the
increase in elasticity and tensile strength of the more
collagenous slow muscles after training suggests that collagen
must undergo some structural changes. In this respect, it is
possible that these changes in the mechanical properties of
slow muscles are related to stabilisation of the reducible
cross-links of collagen (Kovanen,
1996).
With more specific reference to muscle tissue, it has been
proposed that ST (slow twitch) fibres may be able to sustain
cross-bridge attachments for a longer period than FT fibres
(Bosco et al, 1982). Therefore, the former would utilise the
elastic energy stored in their cross-bridges more efficiently
during slow movements. In addition, this process may be
augmented by the behaviour of the connective tissue in each
given muscle in determining the ability of the slow and fast
muscles to perform different types of work (Kovanen et al,
1984). Slow muscles with their greater content of strongly
cross-linked collagen would then be more adapted to slow
contraction, since the fairly rigid collagenous connective
tissue would resist fast contraction. The less rigid
connective tissue in fast muscle, on the other hand, would
facilitate fast movements with greater changes in form.
The differences noted in the collagenous components of
different muscle types could also imply that a slow muscle can
store relatively more elastic energy in its collagenous tissue
than fast muscle, thereby explaining the efficiency of slow
muscle in postural and endurance tasks.
It is a serious omission that most texts focus more on the
effect of different training programmes on muscle than on the
collagenous tissues, because many animal studies have shown
that physical training also strengthens the attachments of
tendons and ligaments to bone. Trained ligaments are thicker
and heavier, though the increase in mass is not necessarily
associated with greater concentration of collagen, a process
which is still poorly understood. In this regard, controlled
strain on the soft tissues may increase the formulation of
fibres in them, thereby contributing to enhanced elasticity
and strength.
Regular resistance training produce not only muscle
hypertrophy, but also an increase in the collagen content of
the ligaments and the connective tissues that surround the
muscle fibres (Tipton et al, 1975). At the same time, the
activity of an enzyme involved with collagen synthesis is
increased by training, an effect which may be stimulated by
lactic acid production during exercise (Booth & Gould, 1975).
It should be noted, however, that moderate intensity treadmill
training of rats produces neither muscle hypertrophy nor
increased growth of intramuscular connective tissue.
Prolonged, low intensity training evidently suffices to
condition the cardiovascular system significantly, but not the
musculoskeletal system. Apparently it is anaerobic, muscle
endurance training which has the most pronounced effect on
enhancing the concentration and strength of collagenous tissue
and its junction zones. Progressive stretching regimes in
conjunction with this type of training would then be seen to
be especially valuable as a component of all sports
preparation.
In contrast to chronic training, single exercise sessions,
occasional stretching or sprint training do not produce
significant increase in junction strength, although sprinting
produces marked increases in ligament mass and concentration
(Tipton et al, 1974). Then, just as ligaments become stronger
and stiffer when subjected to increased stress, so they become
weaker and less stiff with decreased stress, immobilisation
and inactivity (Tipton et al, 1970). The similar changes noted
with ageing may be due not only to the degenerative process
but also to inactivity.
In the light of the above analysis the choice of stretching
regime must also take into account the subject's state of
training, age and health. Furthermore, alteration in hormonal
balance during pregnancy, menstruation and administration of
exogenous hormones (such as anabolic steroids and cortisone)
can affect the mechanical characteristics of collagenous
tissue, so that stretching techniques should be adjusted
accordingly (Viidik,
1997).
So, we can now see that stretching involves much more than is
intimated by the popular workshops and magazine articles --
and science still has many more mysteries to unravel in regard
to the adaptation of soft tissues to loading and the way in
which muscles and extensible tissues interact to produce
efficient movement.
<A lengthened muscle is a strengthened muscle.>
*** On the contrary, if stretching leads to a regular increase
in muscle length, then it may not be able to produce greater
force, since the process is one of optimisation, not
maximisation. The ability of a muscle to exhibit strength,
i.e. produce force, also depends on how its tendinous
attachment inserts into the bones comprising a given joint and
the positioning of that joint (and its neighbours) in space.
<The longer the anatomical length between the actin myosin
filiments the greater contractability of the muscle fibers.
Therefore, stretching and flexibility will gain more
strength.>
*** There is no "length" between the actin and myosin
filaments; they are juxtaposed alongside and among one
another, with the minute "heads" on the myosin filaments
forming cross bridges to active sites on neighbouring actin
filaments -- so, what do you mean by "the longer the
anatomical length between the actin myosin filiments (sic) the
greater contractability (sic) of the muscle fibers"? Also,
what do you mean by "stretching and flexibility will gain more
strength"? Stretching doesn't gain strength, nor does
flexibility, especially since flexibility is a synonym for
"Range of Movement" of a joint (not a muscle).
What Alexandre was referring to undoubtedly was research which
showed that the strength of certain muscles in birds was
increased by hanging loads on their wings for several days at
a time, not a few seconds or minutes of popular fitness class
stretches. While some of this work has been replicated in
animals, it has not been confirmed in humans yet.
However, some research into the acute effects of stretch on
strength production is noteworthy. For example, the rate of
decay of torque following stretch does not depend upon stretch
variables and the absence of significant changes in EMG
(electrical) activity suggests that reflex activity does not
account for the observed changes when large initial forces are
involved. Time-constants of decay are much greater than
time-constants of rise of isometric torque at the same muscle
length, indicating that interaction of series elastic
(connective tissue such as tendons) and contractile elements
is not the sole cause of prolonged torque following stretch.
Thus it seems that stretch temporarily enhances the intrinsic
contractile properties of human muscle, rather than the
nervous processes alone (Thomson & Chapman,
1988).
To examine the effects of strength training on "muscle", we
must remember that the muscle complex consists of both
contractile (actin-myosin) and non-contractile (collagenous
and elastic) components, so that what we are imposing on the
contractile components, we are also imposing on the n
on-contractile components. In this respect, animal studies
have produced the following findings regarding the effect of
exercise or inactivity on the connective or collagenous
tissues (see Chs 1 & 3 of Mel Siff's "Supertraining" for
greater detail about stretching science):
1989. Single exercise sessions and sprint training do not
produce significant increase in junction strength,
although sprinting produces marked increases in ligament
mass and in ratios of mass per unit length (Tipton et
al, 1967; Tipton et al, 1974). Hence, Tipton and
colleagues have concluded that junction strength changes
are intimately related to the type of exercise regime
and not solely to its duration.
1990. Regular endurance training can significantly increase
junction strength-to-bodymass ratios for ligaments and
tendons (Tipton et al, 1974; Tipton et al, 1975).
1991. Long-term endurance exercise programmes cause
significant increases in the junction strength of
repaired injured ligaments (Tipton et al,
1992). In this regard, Tipton et al (1975) suggested that an
increase in tissue capillarisation associated with
chronic exercise may enhance the availability of
endogenous hormones and stimulate blood flow to the
repairing tissue.
1993. Long-term training significantly increases the collagen
content of ligaments (Tipton et al, 1970).
1994. Ligaments become stronger and stiffer when subjected to
increased stress, and weaker and less stiff when the
stress is decreased (Tipton et al, 1970; Noyes, 1977).
1995. Ageing reveals changes in collagenous tissues similar to
those caused by immobilisation, with reduction in
strength and stiffness of ligaments occurring with
advancing age. These changes may be due not only to the
degenerative process, but also to reduced physical
activity, superimposed disease states and other
unidentified processes (Frankel & Nordin, 1980).
Studies of the mechanical and biochemical properties of
tendon reveal a close relationship between tensile strength
and the amount of collagen. Similarly, the concentration of
total collagen is higher for slow muscle than for fast
muscle. This difference also appears at the level of
individual muscle fibres, with the concentration of collagen
in slow twitch fibres being twice that in fast twitch fibres
(Kovanen et al, 1984).
For example, muscle endurance training increases the tensile
strength of both slow and fast muscles, as well as the
elasticity of the former (Kovanen et al, 1984). Other studies
have shown that prolonged running also increases the
concentration of collagen in tendon and the ultimate tensile
strength of tendon (Woo et al, 1981). This finding is relevant
to the limited prescription of off-season transitional or
general physical preparation (GPP) training.
In contrast with this finding, the concentration of collagen
in muscle is not altered by endurance training. However, the
increase in elasticity and tensile strength of the more
collagenous slow muscles after training suggests that collagen
must undergo some structural changes. In this respect, it is
possible that these changes in the mechanical properties of
slow muscles are related to stabilisation of the reducible
cross-links of collagen (Kovanen,
1996).
With more specific reference to muscle tissue, it has been
proposed that ST (slow twitch) fibres may be able to sustain
cross-bridge attachments for a longer period than FT fibres
(Bosco et al, 1982). Therefore, the former would utilise the
elastic energy stored in their cross-bridges more efficiently
during slow movements. In addition, this process may be
augmented by the behaviour of the connective tissue in each
given muscle in determining the ability of the slow and fast
muscles to perform different types of work (Kovanen et al,
1984). Slow muscles with their greater content of strongly
cross-linked collagen would then be more adapted to slow
contraction, since the fairly rigid collagenous connective
tissue would resist fast contraction. The less rigid
connective tissue in fast muscle, on the other hand, would
facilitate fast movements with greater changes in form.
The differences noted in the collagenous components of
different muscle types could also imply that a slow muscle can
store relatively more elastic energy in its collagenous tissue
than fast muscle, thereby explaining the efficiency of slow
muscle in postural and endurance tasks.
It is a serious omission that most texts focus more on the
effect of different training programmes on muscle than on the
collagenous tissues, because many animal studies have shown
that physical training also strengthens the attachments of
tendons and ligaments to bone. Trained ligaments are thicker
and heavier, though the increase in mass is not necessarily
associated with greater concentration of collagen, a process
which is still poorly understood. In this regard, controlled
strain on the soft tissues may increase the formulation of
fibres in them, thereby contributing to enhanced elasticity
and strength.
Regular resistance training produce not only muscle
hypertrophy, but also an increase in the collagen content of
the ligaments and the connective tissues that surround the
muscle fibres (Tipton et al, 1975). At the same time, the
activity of an enzyme involved with collagen synthesis is
increased by training, an effect which may be stimulated by
lactic acid production during exercise (Booth & Gould, 1975).
It should be noted, however, that moderate intensity treadmill
training of rats produces neither muscle hypertrophy nor
increased growth of intramuscular connective tissue.
Prolonged, low intensity training evidently suffices to
condition the cardiovascular system significantly, but not the
musculoskeletal system. Apparently it is anaerobic, muscle
endurance training which has the most pronounced effect on
enhancing the concentration and strength of collagenous tissue
and its junction zones. Progressive stretching regimes in
conjunction with this type of training would then be seen to
be especially valuable as a component of all sports
preparation.
In contrast to chronic training, single exercise sessions,
occasional stretching or sprint training do not produce
significant increase in junction strength, although sprinting
produces marked increases in ligament mass and concentration
(Tipton et al, 1974). Then, just as ligaments become stronger
and stiffer when subjected to increased stress, so they become
weaker and less stiff with decreased stress, immobilisation
and inactivity (Tipton et al, 1970). The similar changes noted
with ageing may be due not only to the degenerative process
but also to inactivity.
In the light of the above analysis the choice of stretching
regime must also take into account the subject's state of
training, age and health. Furthermore, alteration in hormonal
balance during pregnancy, menstruation and administration of
exogenous hormones (such as anabolic steroids and cortisone)
can affect the mechanical characteristics of collagenous
tissue, so that stretching techniques should be adjusted
accordingly (Viidik,
1997).
So, we can now see that stretching involves much more than is
intimated by the popular workshops and magazine articles --
and science still has many more mysteries to unravel in regard
to the adaptation of soft tissues to loading and the way in
which muscles and extensible tissues interact to produce
efficient movement.