Muscle Response to Training

How well do you know your muscles?<b>Hypertrophy</b>

Hypertrophy is the growth in muscle, in response to overload training
occurring primarily as an enlargement of the individual fibres
(Luithi, Howald, Claasen et al, 1986;Gollnick, Timson, Moore & Reidy,
1981; Frontera, Meredith, O'Reilly & Evans, 1988). As a result the
force generated by the muscle can be related to the cross sectional
area (Luithi, et al 1986, Gollnick, et al 1981). Studies have shown
that in the untrained state the percentages of fibre types are similar
to trained subjects, however, the trained subjects exhibited a
preferential hypertrophy of the Type II fibres (Macdougall, Sale,
Alway, & Sutton, 1984; Gollnick, et al 1981; Alway , MacDougall, Sale,
Sutton & McComas, 1988). The amount of hypertrophy is dependant upon
heredity and the amount of training (Thompson, 1994; Hopp, 1993;
Staron, Hikida, Hagerman, Dudley & Murray, 1983), and as a result many
studies have differing figures for the hypertrophy of the muscle
fibres.

For instance, Macdougall et al ( 1976) demonstrated an 11% increase in
arm circumference following a 5 month training regime, and Frontera et
al (1988) demonstrated a 9.3% increase in the cross sectional area of
the quadriceps muscle of the men after 12 weeks of training.This fibre
hypertrophy is very exercise specific as shown by Gollnick, Armstrong,
Saltin, Saubert, Sembrovich and Shepherd (1973), whereby after a 5
month endurance training programme, the cross sectional area of the
Type I fibres was increased by 23%.

Further to this Staron et al (1984), showed that the specificity of
sport had an effect on the preferential hypertrophy of fibre types
with his study comparing runners and weight lifters to non-exercising
controls. Tesch & Karlsson (1985), furthered this by comparing the
Deltoid and Vastus Lateralis of runners, kayakers, wrestlers and
weightlifters (Fig.2). Not surprisingly the area of Type II fibres in
the weightlifters were significantly more hypertrophied in the Vastus
Lateralis muscle than the other groups, followed by wrestlers, and
surprisingly, kayakers. Runners had the smallest area for both Deltoid
and Vastus lateralis muscles and the highest cross sectional area of
Type I fibres for the Vastus Lateralis when compared to the Deltoid.
The weightlifters were the only group to have equal Type I area for
both muscles.

Fig.2. Relationship between muscle fibre type distribution in vastus
lateralis and deltoid (Tesch and Karlsson, 1985).

The mechanism behind hypertrophy is due to synthesis and thickening of
myofibrils and increase in their number. Further to this, as
resistance training increases the number of sarcomeres increase as the
synthesis of protein increases, and the breakdown of protein
decreases (Bandy & Dunleavy, 1996). This acceleration of the protein
synthesis is directly dependant upon the increased tension
that the muscle is required to generate during exercise (Bandy &
Dunleavy, 1996).

<b>Hyperplasia</b>

Another means hypothesized by which muscle can increase in size during
intense training, is by hyperplasia or fibre splitting. It has been
suggested that once the fibre has reached maximum hypertrophy any
further strength or size gains can come only from formation of two
daughter cells through lateral budding, or longitudinal fibre splitting
(Gonyea & Erickson, 1976; Gonyea, 1980).

Although work on animal species suggest that hyperplasia is an active
component of muscle adaptation to exercise (Gonyea & Erickson, 1976;
Gonyea, 1980), little has been shown to support this in a human model.

One study, used insulin-like growth factor to bring about increases in
peptide growth factions which precede muscular cell proliferation and
differentiation (Devold, Rotwein, Sadow Novakovski & Bechtel, 1990).

Therefore with this and the animal studies it has been suggested that
gene alteration due to muscular tension can occur, resulting in the
formation of new muscle fibres (Vujnovich, 1995). Comparisons of
animal studies to humans, however, are flawed in that animals have a
limited capacity for muscle cell hypertrophy (Bandy & Dunleavy, 1996).
As a result fibre splitting or hyperplasia may be the only means of
coping with muscular overload.

Researchers tend to agree that an increase in cross sectional area of
muscles following training is mainly due to hypertrophy (Luithi et al
1986; Gollnick et al, 1981; Frontera et al, 1988; Macdougall et al,
1984, Alway et al, 1988; Staron et al, 1984).

<b>Gender Differences</b>

It has been shown that, preferential hypertrophy occurs in Type II
compared to Type I fibres as a result of resistance training (Alway et
al, 1988; Macdougall et al, 1984,).In one study comparing biceps of
male and female bodybuilders it was found that the relative amount of
Type I fibres was comparable, however, the ratio of Type II to Type I
fibres in the male group was much higher suggesting greater
preferential hypertrophy of Type II fibres in males (Alway et al,
1989).

Another study by Willmore (1974), showed that hypertrophy of muscle in
females was less when compared to males. Further to this the percentage
increase in strength was slightly greater in females. The speculations
behind this, have attributed the amount of hypertrophy in the male, to
the 20-30 times more testosterone (Bandy & Dunleavy, 1996). Other
factors to consider are the pretraining strength of females, as well as
the smaller cross sectional area of muscles, and the presence of
subcutaneous fat in the female athlete when compared to her male
counterpart (Alway et al, 1989, Bandy & Dunleavy, 1996).

<b>Muscle Fibre Type</b>

Several studies have shown no significant change in the fibre types of
human muscle following either endurance resistance training on muscle
(Gollnick et al, 1973; Thorstensson, Grimby & Karlsson, 1976)
furthering the belief that muscle fibre type distribution is
genetically determined. However, the training periods for these studies
appeared too short, and of an intensity not high enough to elicit a
response. It should be remembered that elite athletes train at
extremely high levels for many years. (Howald, 1982).

It has been shown that with a change in training work load from
continuous to intermittent paralleled a decrease in the Type I fibres
with a proportional increase in Type IIc or transitional fibres
(Jansson et al, 1978). Further to this a possible conversion of Type
IIb to Type IIa has been demonstrated with intensive endurance training
(Andersen & Henriksson, 1977a), through the intermediate high
frequency, intermediate fatique resistant Type IIx fibres (Thompson,
1994).

It has also been demonstrated that the Type II fast twitch fibres have
been transformed to Type I slow twitch fibres with electrical
stimulation of 10Hz (Leiber, 1992). The transformation begins with
increases in percent of mitochondria, oxidative enzyme activity,
capillaries per square millimetre, total blood flow and consumption.
There is an increase in the percentage of fast oxidative glycolytic
fibres at the expense of fast glycolytic fibres (Leiber, 1992).

The amount of calcium ATPase decreases, as is evident in the prolonged
time to peak twitch tension and relaxation (Essen, Jansson, Henriksson,
Taylor & Saltin, 1975). After approximately 4 weeks of continuous
stimulation, the myosin light chain profile changes from containing
fast fibre light chains to light chains characteristic of slow fibres.
Furthering this, the new slow fibre light chain synthesizes heavy
chains to be incorporated in the myosin filament. By this time the
former fast twitch Type II fibre resembles a slow twitch Type I fibre
in every respect (Leiber, 1992).

<b>Capillarisation</b>

It has been discussed that specificity of training results in specific
responses, for instance, endurance training will result in a marked
increase in oxidative enzymes. Along with this, comes an increase in
capillary density (Andersen & Henricksson 1977b).

Klausen, Andersen and Pelle (1981) demonstrated that following an
intensive endurance bicycle training for 8 weeks there was
considerable proliferation of the capillary network. The number of
capillaries per millimetre increased by 22%, and the capillaries
per fibre by 20%. The capillary number differed for each fibre with
Type I increasing by 24%, Type IIa by 20% and Type IIb by 30%. There
was also a 10-15% decrease in the fibre area per capillary. These
results were consistent with those demonstrated by Andersen &
Henricksson (1977b). Further to this, during a detraining period of 8
weeks these trends were reversed (Klausen et al, 1981).

<b>Enzyme Activity</b>

Periods of endurance training have been demonstrated to increase the
activity of oxidative enzymes, Succinate dehydrogenase and cytochrome
oxidase, which was accompanied by an increase in the VO2 max (Klausen
et al, 1981). Surprisingly an increase in endurance training can also
lead to increases in the glycolytic enzyme phosphofructokinase
(Gollnick et al, 1973). Conversely, with detraining the levels of both
oxidative and glycolytic enzymes decreased.

The amount of change in the enzyme activity is highly dependant on the
type of activity with glycolytic enzymes responding best to short
bursts of maximal effort and oxidative enzymes to endurance training.


<b>Immobilisation-Atrophy</b>

In opposition to hypertrophy following training, the result of
immobilisation is atrophy. The signs of muscle atrophy are decreases in
size, muscle strength and endurance (Bandy & Dunleavy, 1996). Atrophy
can occur due to pathology, malnutrition, denervation or from disuse.

Following immobilisation, the decrease in cross sectional area and
decrease in percentage of type I fibres (Jakobsson, et al, 1992)
can lead to abnormal movement patterns, increased stress on joints and
increased risk of injury, as well as extracellular fluid accumulation
and connective tissue alterations (Bandy & Dunleavy, 1996).

Histologically, animal studies show that atrophy can result from a
decrease in the rate of protein synthesis and an increased rate of
protein catabolism (Watson, Stein & Booth, 1984). There is specific
catabolism of myofibrillar proteins, with Type I myosin being affected
in preference to Type II myosin levels (Jakobsson et al, 1992).

<b>Fibre Type</b>

As mentioned before, immobilisation due to disuse causing hypokinesia,
will result in greater atrophy of type I fibres than type II fibres.
Therefore the muscles with a large amount of type I fibres will be most
susceptible to immobilisation. These are the postural or tonic muscles,
therefore functional tasks such as standing, will be significantly
affected for extended periods of time (Bandy & Dunleavy, 1996).

In contrast, atrophy associated with muscular pathologies i.e.,
Muscular Dystrophy, result in preferential atrophy of the Type II
fibres (Wheeler, 1982).

<b>Aging</b>

The aging process as with nearly every bodily function is extremely
variable from person to person (Hopp, 1993; Thompson, 1994). In
physical terms, aging is associated with slowed movements, a decrease
in muscle strength and force production, and loss or decrease in fine
motor control. Although the symptoms of muscular atrophy are evident,
decline in muscle strength and decreased independence due to frailty
are commonly seen, little is known as to the exact cause.

Several studies have been performed concerning the biochemical changes,
distribution of fibre types, muscle atrophy, fibre number and size.

<b>Biochemical</b>

Within the studies there appears to be some agreement. Most show that
there is no statistical difference in the glycolytic enzymes such as
phosphofructokinase, lactate dehydrogenase in the aging human when
compared to the younger counterpart ( Larson & Karlsson 1978, Larson,
Sjodin & Karlsson, 1978). Further to this, Essen-Gustavson & Borges
(1986), found that although the glycolytic enzymes were lower in Type I
when compared to Type II fibres, a comparison of the glycolytic enzymes
in the fibres showed no difference between young and older subjects.
Larson et al (1978) showed that age did not have an adverse affect on
the mitochondrial activity of the fibre.

In contrast, one study found the oxidative muscle enzyme activity to be
about 25% lower in the older subject in comparison to the younger group
(Coggan, 1992, cited in Thompson, 1994). One reason given for this is
the differing level of physical activity.

In fact, it seems that the major factor influencing glycolytic enzyme
capacity and, although investigated to a lesser extent, oxidative
enzymes in relation to age, is the level of physical activity
(Thompson, 1994).

During aging, the proportion of Type I and Type II fibre types seems to
alter (Larsson et al, 1978).

The percentage of Type I fibres taken from the Vastus Lateralis muscle
seemed to alter from 39% in 20-29 year old to a higher percentage of
66% in the 60-66 year old. From the third to the seventh decade the
proportion of Type II fibre seemed to decrease in a linear manner,
however the Type II subtypes remained unaltered. (Larsson & Karlsson,
1978).

Possible reasons for this proliferation of the Type I fibres with aging
include splitting or new fibre formation, preferential atrophy or
transformation of Type II to Type I through the Type IIc fibre
(Larsson, 1978; Larsson et al, 1978).

However, recent studies on pectoralis muscles showed that the Type I
fibre percentage remained unchanged with age (Sato et al, 1983, cited
in Thompson, 1994).

Many researchers have found that the distribution and percentage of
muscle fibre has more to do with the level of physical activity,
and heredity rather than the aging process (Larsson, 1978; Larsson et
al, 1978; Lexell, Downham &Sjostrom, 1986).

<b>Muscle Atrophy</b>

Muscle atrophy can be expressed in terms of the muscle fibre size and
muscle fibre number.

<b>Muscle Fibre Size</b>

The fibres, when at the maximal size (20-30 years of age) (Thompson,
1994), have cross sectional areas, whereby the Type II fibres have
areas 15-20% in excess of Type I fibres (Lexell, Taylor & Sjostrom,
1988). During the seventh decade, however, the fibre sizes will be
approximately equal (Lexell et al,1986). As age increases, so the size
of the Type II fibres, and in particular the Type IIb fibres decreases
(Lexell et al, 1988)

<b>Muscle Fibre Number</b>

With many animal species a decrease in fibre number has been shown with
aging. (Thompson, 1994). In human studies, using mainly the Vastus
Lateralis muscle, the older group were found to have both fibre number
and total muscle size to be smaller than their younger counterparts
(Larsson et al, 1978; Lexell et al, 1986; Lexell et al, 1988).

Therefore a combined effect of both the decrease in the size of the
fibre, and in particular the size of Type IIb fibres, and the number of
fibres add to affect the amount of age related muscle atrophy. Once
again, this phenonmenon is largely related to heredity and the level of
physical activity (Hopp, 1993; Thompson, 1994).

<b>Conclusion</b>

In summary, muscles are dynamic functional units. They function in
accordance to their structure, and they also respond by altering their
structure according to the functional demands. For instance, a trained
muscle will hypertrophy in accordance to its training and an
immobilized muscle will atrophy.

It seems that with the right training of muscle Type IIb can be
converted to Type IIa (Andersen & Henricksson, 1977a), and Type I can
decrease with a relative increase in Type IIc (Jansson et al, 1978).

However, it is impossible to be able to predict performance on the
grounds of hypertrophy or percentage of muscle types. Due to the
complexity of most functional and sporting activities there are a
number of physiological and psychological factors that comprise each
performance, therefore muscle fibre type is just one small piece of an
extremely complex jigsaw (Howald, 1982).



<b>Short Answer Review Questions</b>

Provide values for percentage of type I fibres for Vastus Lateralis,
Biceps Femoris, Tibialis Anterior, Soleus, Deltoid, Supraspinatus,
Infraspinatus, Erector Spinae, Rectus Abdominus, Vastus Medialus
Obliquus, Triceps, and Orbicularis Oculi.

Provide average values for percentages of type I fibres in Vastus
Lateralis muscles of runners, sprinters, weightlifters, canoeists,
cyclists and soccer players.

Briefly describe the formation of muscle fibres from conception to
birth.

Discuss mechanisms of muscle growth in response to training.

Describe the effects of electrical stimulation to muscles. How does
this differ from training effects?

Discuss the effects of aging on the muscle fibre.

Discuss the statement that 'Sprinters are born and not made', and
why this may not be true.

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