CHAPTER 8

Chronic adaptations
to training

Whenever an individual engages in training there are placed upon it and are referred to as chronic
two types of physiological responses that their body adaptations to training. The combined effect
produces as a result of the demands of the exercise. of all chronic adaptations is known as the
These are: training effect.
• Immediate, short-term responses that last only This chapter examines the chronic adaptations to
for the duration of the training or exercise session training, that occur at the system (circulatory and res-
and for a short time-period afterwards (recovery). piratory) level and the tissue (muscular) level.
These are commonly referred to as acute responses Acute responses were covered in year 11 and are
to exercise. not directly assessed in the year 12 course. However,
• Long-term responses that develop over a period it may be useful to briefly revise these concepts as
of time (usually a minimum of six weeks) when they provide a solid grounding for a complete under-
training is repeated regularly. These responses standing of chronic adaptations (refer to chapters 5
involve the body adapting to the new demands and 6, Live it up 1, second edition).

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 Assessment tasks
Task Topic Page
Data analysis Trained and untrained heart-rate responses (activity 1) 253
exercise
Case study analysis Lance Armstrong (activity 2) 255
Written reports The ‘training effect’ (activity 3) 263
Chronic adaptations to a training program (activity 4) 264

After completing this chapter, students should be able to:

CHAPTER 8
• identify and summarise the chronic adaptations
to aerobic and anaerobic training that occur
at the system (circulatory and respiratory) level
and tissue (muscle) level.

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 Chronic training adaptations
Exercise or training undertaken regularly over an extended period of
time (usually at least three times per week for a minimum of 6–8 weeks)
leads to the development of long-term or chronic adaptations to training.
Some of these adaptations are evident when an individual is at rest and others
can be measured when the body is engaged in exercise or activity. Some
adaptations are apparent when the individual is working at sub-maximal
exercise intensities, whereas others are evidenced when the individual is
engaged in maximal exercise. Once achieved, these adaptations are retained
unless training ceases. Upon cessation, the body will gradually revert to its
pre-training condition. This process is referred to as ‘de-training’ or revers-
ibility (see chapter 7).
Unlike acute responses to exercise, chronic adaptations to training vary
greatly and are dependent upon:
• The type and method of training undertaken — basically aerobic
(endurance) training as opposed to anaerobic training. Chronic training
responses are very specific to the type of training performed.
• The frequency, duration and intensity of the training undertaken — the
greater the frequency, duration and intensity of training, the more pro-
nounced the adaptations. However, factors such as overtraining (see
chapter 9) and the principle of ‘diminishing returns’ (see chapter 7) need
to be considered in relation to this.
• The individual’s capacities and hereditary factors (genetic make-up)
— such as muscle fibre-type distribution (fast-twitch as opposed to
slow-twitch fibres). According to some research 97 per cent of these are
genetically determined.
Chronic training adaptations may occur at both the system level, particu-
larly the cardiovascular and respiratory systems, and/or at the tissue level
that is, within the muscles themselves.

Chronic adaptations to aerobic

(endurance) training
The minimum period for chronic adaptations to occur with endurance or
aerobic training is six weeks, although they are more evident after twelve
weeks. These adaptations can occur at both the tissue and systems levels.

Cardio-respiratory adaptations to aerobic

(endurance) training
Chronic cardio-respiratory adaptations to aerobic training are primarily
designed to bring about the more efficient delivery of larger quantities of
oxygen to working muscles. These are particularly significant because they
profoundly decrease the risk of developing cardiovascular disease and other
health-related illnesses.
Cardio-respiratory adaptations are best developed through continuous,
fartlek and longer-interval type training. They include:
• cardiac hypertrophy (increased ventricular volume)
• increased capillarisation of the heart muscle
• increased stroke volume of the heart
• lower resting heart rate
• lower heart rate during sub-maximal workloads
• improved heart-rate recovery rates
• increased cardiac output at maximum workloads
• lower blood pressure

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 • increased arterio-venous oxygen difference (a-VO2 diff)
• increased blood volume and haemoglobin levels
• increased capillarisation of skeletal muscle
• changes to blood cholesterol, triglycerides, lipoprotein levels (low- and
high-density)
• increased lung ventilation
• increased maximum oxygen uptake (VO2 max)
• increased anaerobic threshold.

Figure 8.1 (a) and (b): Cardiovascular adaptations

Effects of aerobic training
on cardiac hypertrophy Cardiac hypertrophy
following intense, sustained Sustained aerobic training results in the enlargement of the heart muscle
aerobic training. The size of the itself. This enlargement is referred to as cardiac hypertrophy. In endur-
ventricular cavities, particularly ance athletes, an increase in the size and therefore volume of the ventricular
the left ventricle, increases. chambers, particularly the left ventricle, occurs (figure 8.1). This in turn sig-
nificantly increases stroke volume.

(a) Untrained individual (b) Trained endurance athlete

Note: Enlarged left ventricle

Increased capillarisation of the heart muscle

Cardiac hypertrophy also leads to an increase in the capillarisation of the
heart muscle itself. In other words, there is an increase in the capillary
density and blood flow to the heart muscle itself (figure 8.2). The increased
supply of blood and oxygen allows the heart to beat more strongly and
efficiently during both exercise and rest. This also results in a coronary pro-
tective benefit, that is a decreased risk of heart attack.
(a) (b)
The two
coronary
arteries

Figure 8.2 (a) and (b):

Capillarisation (blood supply) to
the heart before (a)
and after (b) a long-term
aerobic training program

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 Increased stroke volume of the heart

Rest — trained and untrained athl

The increased hypertrophy of the heart leads to a significant increase in the

Maximal exercise — untrained

145 heart’s stroke volume. In other words, it ejects a greater volume of blood
Stroke volume (mL/beat)

Maximal exercise — trained

with each beat. Stroke volume is greater at rest, during sub-maximal exer-
130 cise and during maximal workloads for a trained athlete, compared to an
untrained person. For example, the average stroke volume at rest for an
115
untrained male is about 70–80 millilitres/beat, whereas trained male endur-
ance athletes may have stroke volumes at rest of 100 millilitres/beat or
more. During maximal exercise these values may increase to about 110 mil-
100
lilitres/beat for an untrained person, and 130 millilitres/beat for a trained
athlete. Elite endurance athletes may have values as high as 190 millilitres/
0
beat (figure 8.3). Trained and untrained females have lower stroke volumes
Figure 8.3: than their male counterparts under all exercise conditions, mainly due to
Stroke volume in response to their smaller heart size.
aerobic training. Stroke volume
is greater for trained endurance Lower resting heart rate
athletes at rest and at all The amount of oxygen required by an individual while at rest basically does
exercise intensities. not alter as a result of their training status. At rest, it takes about 5 litres
of blood per minute (cardiac output) to circulate around the body in order
to supply the required amount of oxygen to the body cells (whether the
individual is trained or untrained). We should remember at this point, that
cardiac output (Q) is equal to stroke volume (SV) multiplied by heart rate
(HR):
Q = SV × HR
However, if an individual has developed a greater stroke volume,
the heart does not have to beat as frequently to supply the required blood
flow (and oxygen). For example:
Before training:
Q = SV × HR
5 L/min = 70 mL/beat × 71 beats/min
After training:
Q = SV × HR
5 L/min = 100 mL/beat × 50 beats/min
It is for this reason that the resting heart rate is a useful indicator of aerobic
fitness. Generally, the lower the resting heart rate, the greater the individu-
al’s level of aerobic fitness. It may be as low as 35 beats per minute for elite
endurance athletes such as marathon runners, triathletes, road cyclists and
distance swimmers, compared to the average resting heart rate of around
70 beats per minute for an average adult male.

Lower heart rate during sub-maximal workloads

Trained aerobic athletes have lower heart rates at sub-maximal workloads
compared with those of untrained individuals. This is mainly a result of
their increased stroke volume, which means that more blood is pumped
with each beat of the heart, and therefore the heart does not have to work as
hard to supply the required blood flow and oxygen supply. Put quite simply,
the heart works more efficiently. Regular aerobic training also results in a
slower increase in heart rate during exercise and a lower and faster attain-
ment of a steady state during exercise. Figure 8.4 opposite clearly indicates
the training effect on heart-rate response to sub-maximal workloads.

Improved heart-rate recovery rates

The heart rate of a trained athlete will return to pre-exercise levels
(resting rate) in a much shorter time than that of an untrained individual
(figure 8.4).

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 Figure 8.4: 165
Heart-rate responses before,

 

 



 
during and after sub-maximal 145
exercise for a trained athlete
125
and an untrained individual. Note
that the heart-rate response of a 105
Trained athlete (B)
trained endurance athlete (B)
is lower than that of an 85
untrained person (A) at rest
65
and at all exercise intensities.
The heart rate of a trained athlete
Rest Moderate Recovery
also returns to resting values work
more quickly upon cessation
of exercise compared
with an untrained person. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26






 

Key knowledge Activity 1 Data analysis exercise

• Chronic adaptations of
the cardiovascular, Trained and untrained heart-rate responses
respiratory and muscular
systems to training Refer to figure 8.4 and answer the following questions:
a What is B’s heart-rate response from minute 6 to minute 18?
b What term describes B’s heart-rate pattern from
Key skill minute 12 to minute 17?
• Summarise accurately c Why does the heart rate remain above resting levels from
information in relation to minute 18 to minute 26?
chronic adaptations to d What are three physiological parameters that B has developed
training. more fully than A? Explain how each parameter resulted in lower
heart rates for B.
e Why does B have a lower resting heart rate than that of A? Give
the physiological reasons, using the terms ‘stroke volume’,
‘hypertrophy’ and ‘left ventricle’.
f Why do both A and B have an increase in heart rate from
minute 5 to minute 6?
g Which energy system produced the majority of energy for this
exercise bout? Justify your selection in terms of intensity and
duration of activity.

Figure 8.5:
Cardiac output at rest Increased cardiac output at maximum workloads
and at maximal exercise
While cardiac output remains unchanged at rest and even during sub-
for trained and untrained subjects
maximal exercise regardless of training status, it does increase during
30 maximal workloads. During maximal exercise, cardiac output may increase
to values of 20–22 litres per minute for untrained males and 15–16 litres per
Rest — trained and untrained athletes

25 minute for untrained females.

Cardiac output (L/min)

By contrast, highly trained athletes have recorded values exceeding

Maximal exercise — untrained

20 30 litres per minute (figure 8.5).

Maximal exercise — trained

15 Lower blood pressure

An aerobic training program may lower blood pressure, especially among
10 people who suffer from hypertension (high blood pressure). Both systolic
and diastolic pressure levels may decrease during both rest and exercise as a
5 result of training. This helps to reduce resistance to blood flow and reduces
strain on the heart, thereby decreasing the risk of heart attack and other car-
diovascular conditions.

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 Increased arterio-venous oxygen difference
Trained individuals are able to absorb more oxygen from their bloodstream
into their muscles during exercise performance, as compared to untrained
subjects. This is due to increased muscle myoglobin stores and an increased
number and size of mitochondria within their muscles. As a result of this, the
concentration of oxygen within the venous blood is lower, and subsequently
the arterio-venous oxygen difference is increased during both sub-maximal
and maximal exercise. Therefore, an increased arterio-venous oxygen
difference (a-VO2 diff) indicates a greater uptake of oxygen by the muscles
within trained individuals.

Increased blood volume and haemoglobin levels

Regular and sustained aerobic training may lead to total blood volume rising
by up to 25 per cent (from 5.25 litres to 6.6 litres) for an average adult male.
As a result, red blood cells may increase in number and the haemoglobin
content and oxygen-carrying capacity of the blood may also rise.

Increased capillarisation of skeletal muscle

Long-term aerobic training leads to increased capillarisation of skeletal
muscle. The average number of capillaries supplying each muscle fibre is 5.9
for trained athletes compared with 4.4 for untrained individuals.

Changes to blood cholesterol, triglycerides, low- and

high-density lipoprotein levels
Regular aerobic training may result in a decrease in blood cholesterol levels,
triglycerides and low-density lipoprotein (LDL). These substances are asso-
ciated with the development of coronary heart disease. Furthermore, it has
been found that aerobic training increases the ratio of high-density lipo-
protein (HDL) to low-density lipoprotein. High-density lipoprotein is thought
to provide a coronary protective effect, lessening the risk of developing
coronary heart disease.

Respiratory adaptations
Increased lung ventilation
Regular aerobic training results in more efficient and improved lung
ventilation. At rest and during sub-maximal exercise, ventilation may
in fact be reduced due to improved oxygen extraction. However, during
maximal workloads, ventilation is increased because of increased tidal
volume and respiratory frequency. Pulmonary diffusion — the ability
of the blood to extract oxygen from the alveoli — is also enhanced as a
result of training.

Increased maximum oxygen uptake

Aerobic training results in an increase in the maximum oxygen uptake
(VO2 max) during maximal exercise. This improvement can be in the range
of 5 to 30 per cent following a regular and sustained training program.
This improvement comes about because of adaptations such as increases
in cardiac output, red blood-cell numbers, a-VO2 difference and muscle
capillarisation, as well as greater oxygen extraction by the muscles.
Figure 8.6 shows maximum oxygen uptake values for Australian sports
people. Note that highly trained elite-level (national and international) ath-
letes, both male and female, have higher average values than active young
men and women.

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 Figure 8.6:
Treadmill
Approximate maximum oxygen

uptake values of Australian
sportspeople Active young men 50.8
National-level Australian Footballers 53.9
International-level soccer footballers 56.0
National-level volleyball players 56.4
National-level squash players 59.0
International-level field-hockey players 61.4
National-level middle-distance runners 67.0
National-level long-distance runners 73.5
40 50 60 70
mL/kg
min


Active young women 45.4

National-level volleyball players 46.8

National-level field-hockey players 50.1
National-level squash players 51.5
National-level middle-distance runners 62.1
40 50 60 70
mL/kg
min

Increased anaerobic or lactate threshold

As a result of the adaptations that improve oxygen delivery and utilisation
in the muscles, a higher lactate threshold (the point at which oxygen supply
cannot keep up with oxygen demand) is developed. The advantage of this
of course is that the anaerobic glycolysis (lactic acid) system is not utilised as
much until higher exercise intensities are reached. Consequently, lactic acid
and hydrogen ion accumulation will be delayed until these higher work-
load intensities are attained. Put most simply, this means that the athlete can
‘work harder and for longer periods’.

Key knowledge Activity 2 Case study analysis

• Chronic adaptations of
the cardiovascular, Lance Armstrong
respiratory and muscular
systems to training Read the article in figure 8.7 on pages 256–7 and answer the
following questions:
a According to the article, what physiological adaptations does
Key skill Lance Armstrong possess that enabled him to be so successful?
• Summarise accurately
b What other chronic training adaptations might Armstrong
information in relation to
have developed through training? List these under the following
chronic adaptations to
categories:
training.
• muscular parameters
• cardiovascular parameters
• respiratory parameters.
c How would you expect Armstrong to perform on the 20-metre
multi-stage fitness test for aerobic capacity (see chapter 6)?
d Which aerobic-capacity tests might better suit Armstrong?
Explain your answer.

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 Lance Amstrong FUEL FOR
ARMSTRONG’S BODY

heads for triumph in Professional cyclists such as Lance

Armstrong burn 4000 to 6000 calories

the Tour de France during a flat stage and more than 8000
calories during a mountain stage.
Studies say the average human burns
By Mike Van Niekerk between 1400 and 2500 calories a
Tomorrow in Paris, Lance Armstrong Between 1992 and 1999 Coyle day. All that energy has to come from
will call it quits. Barring an acci- had the unique opportunity to test somewhere. Meals during the Tour
dent before the 2005 Tour de France Armstrong’s body and chart how are simple and nourishing. Breakfast
crosses the Champs Elysees finish it adapted to intense training and consists of eggs, pasta, rice, bread,
line, the 33-year-old American will competition. Armstrong was an yoghurt, cereals. During the race,
retire with a seventh straight yellow extraordinary athlete who … dra- lunch is handed to the riders in bags
jersey on his shoulders and a repu- matically improved over time. called musettes. They contain
tation as one of the greatest athletes To do well, Coyle said, cyclists high-carbohydrate items: small
of his generation. needed a big heart, low levels of sandwiches filled with honey and
Watching the devastating ease with lactic acid in their blood — the by- banana slices, cakes, energy bars,
which Armstrong this week matched product of intense exercise — and the energy gells and water or sports drinks.
every attack by his rivals in the steep ability to efficiently generate power, After a stage, team members snack on
climbs of the Pyrenees, you would measured as watts. When Armstrong, cereal and high-protein foods. Dinner
think he was superhuman — and you then 20, first asked Coyle for an analy- consists of meats, pasta, rice, salad,
would be right. Armstrong is a physi- sis of his potential, he already had the bread and dessert.
cal freak, spectacularly well adapted big heart and low lactic acid. But his
to the harsh demands of endurance muscle efficiency was not very good,
bicycle racing. Coyle said. It came in at 21 per cent.
His heart is a third bigger than That first year, two other athletes Stimulated by years of training
average, pumping blood to his we studied were better. Armstrong intensely for up to six hours most
muscles more efficiently; at rest his improved until his career was sus- days, Armstrong’s muscles changed
heart rate is 32 beats a minute, less pended in 1996: he was diagnosed from 60 per cent slow-twitch fibre —
than half the average. His blood is with testicular cancer, which had the kind that doesn’t burn out quickly
more saturated than normal, even for spread to his lungs and brain. Eight — to 80 per cent.
a top-level sportsman, with energy- months after his treatment ended, Clearly, this champion embodies a
producing oxygen; his VO2 max Coyle’s tests found nothing perma- phenomenon of both genetic natural
rating, which measures how much nently wrong with Armstrong. selection and the extreme to which the
oxygen the lungs can consume during The last test was done in 1999, human can adapt to endurance train-
exercise, is 85. An average healthy after Armstrong won his first Tour de ing performed for a decade or more in
male might rate a 40. France. a person who is truly inspired, Coyle
Even in an untrained state, In the previous two years his wrote.
Armstrong is at the same level as a lactic acid had dropped further and Good genes and sheer hard work.
highly trained but less gifted athlete, his efficiency increased to 23 per cent. Armstrong is a driven personality,
according to scientist Edward Coyle. Together with the weight loss during whose attention to detail shocked
Go back to those Pyrenean climbs cancer treatment he was delivering the Europeans. Never had anyone
again. Armstrong can ride uphill 18 per cent more power — meaning reconnoitred every mountain climb
generating about 500 watts of power he could go faster up mountains with months ahead of the tour — ridden
for 20 minutes, something a typical less effort. them repeatedly for training, as well
25-year-old could do for only 30 Coyle’s study, Improved Muscu- as memorised those parts where he or
seconds. A professional hockey player lar Efficiency Displayed as Tour de other riders might attack.
— perhaps even an AFL footballer — France Champion Matures, in the Few, if any, top cyclists have
might last three minutes then throw June issue of the Journal of Applied combined a precision diet to give
up, according to Coyle, director of the Physiology, reveals the combination of themselves exactly the right race-
human performance laboratory at the natural gifts and focused hard work ready weight in July with carefully
University of Texas. that took Armstrong to the top. calibrated training and racing to

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 MARATHON MAN HEART & LUNGS
MUSCLES & BONES A third larger than an average man’s, Armstrong’s heart has a resting
A product of metabolism, lactic acid rate of an astounding 32 beats a minute. At peak exertion, it can race
produces the excruciating burning up to 200 beats a minute. The average human’s resting heart beats 60
sensation familiar to participants in to 80 times a minute. The resting heart rate is the minimum number of
strenuous physical activity. It could beats a minute needed to sustain the body.
be a side effect of his gruelling • LUNGS The average healthy male’s lung capacity uses
training regimen or the 40 millilitres of oxygen per kilogram of body weight
abnormally high percentage of during exercise. Armstrong’s capacity is around 85.
slow-twitch muscles in his body.
Armstrong produces less lactic
STOMACH
acid than normal.
Teammates are responsible for bringing
• THIGH BONE Unusually long,
Armstrong food during the race. Without it,
it allows Armstrong to apply
his body would run out of glycogen — the
more force to the pedals.
short-term supply of carbohydrates stored
• BODY FAT At about 4
in muscles.
or 5 per cent,
Armstrong’s body
fat is so low that he
is more susceptible
to infections.

reach a physical peak at the end of the It’s possible the 102-year-old Tour Foundation for cancer research and
first week of the tour, when the race de France will never again produce awareness.
hits the first mountains. Jan Ullrich, another rider who can win seven In an interview with Outdoor mag-
Armstrong’s most noted challenger times straight. No one has done it azine last month, Armstrong said
for six of the past seven years, is before. that one night recently he drove with
well known to put on weight in the Astonishingly, Armstrong has quit his rock musician girlfriend Sheryl
off season then over-compensate by at the height of his powers. It’s com- Crow past the governor’s mansion in
losing the excess too quickly before monly accepted that on the strength his home town of Austin, the capital
the tour, stressing his system. of this year’s performance, measured of Texas. It’s a nice mansion. Nice
Armstrong has surrounded himself against his rivals, he could likely win place, nice house, he teased. If he
with experts, such as celebrity coach an eighth yellow jersey in 2006. does decide to go into public life, it’s
Chris Carmichael and Italian Michele What he’ll do now is open to spec- certain you will hear the name Lance
Ferrari — although less openly since ulation. Having earned a reported Armstrong in future just as often as
he was implicated in a drugs scandal $36.6 million in 2004 in salary and when he was winning the Tour de
— with whom he daily discusses endorsements, on top of previous France.
training statistics. years’ earnings and with an ongoing
Finally, there is Armstrong’s commercial relationship with the Dis-
Source:
incredible desire to win. Even sur- covery Channel and other sponsors,
The Age, 23 July, 2005
rounded by attacking rivals, as he has he’ll be able to do as he pleases. He
been in this tour, he has never once sat will certainly continue promoting
back when the challenges came. the work of his Lance Armstrong

Figure 8.7:
Case study of an elite athlete’s
adaptations to training

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 Muscle tissue adaptations to aerobic
(endurance) training
Chronic aerobic training adaptations within muscular tissue are best pro-
duced through continuous training or high-repetition resistance training.
The following tissue-level changes can be observed within skeletal muscles
following extensive endurance training:
• increased oxygen utilisation
— increased size and number of mitochondria
— increased myoglobin stores
• increased muscular fuel stores
• increased oxidation of glucose and fats
• decreased utilisation of the anaerobic glycolysis (lactic acid) system
• muscle fibre type adaptations.
A general summary of these muscle tissue adaptations is shown in figure
120 8.9 opposite.
100 Increased oxygen utilisation

 


80
Aerobic training enhances the body’s ability to attract oxygen into the
muscle cells and then utilise it to produce adenosine triphosphate (ATP) for
muscle contraction. This process occurs in the following ways:
Mitochondrial number

60
Glycogen oxidation
Myoglobin content

• Increased size and number of mitochondria. The mitochondria are the

40 sites of ATP resynthesis (see chapter 2), and where glycogen and tri-
Fat oxidation

glyceride stores are oxidised. The greater the number and size of the
20 mitochondria located within the muscle, the greater the oxidisation of
fuels to produce ATP.
0 • Increased myoglobin stores. Myoglobin is the substance in the muscle cell
5 days per 5 days per that attracts oxygen from the bloodstream into the muscle. Aerobic
week for week for
12 weeks 28 weeks
training significantly increases the myoglobin content in the muscle and
therefore its ability to extract oxygen.
Figure 8.8: Figure 8.8 illustrates the effect of aerobic training on these parameters.
Effects of aerobic training on
muscle tissue Increased muscular fuel stores
Aerobic training also leads to increases in the muscular storage of glycogen,
free fatty acids and triglycerides, along with the oxidative enzymes required
to metabolise these fuel stores and produce ATP.

Increased oxidation of glucose and fats

The muscular adaptations already discussed result in an increase in the
capacity of muscle fibres to oxidate both glucose and fats. In other words, the
capacity of the aerobic system to metabolise these fuels is increased (figure
8.8). Furthermore, the increased oxidation of fats as a fuel source — due to
the increased storage of triglycerides and free fatty acids, plus the vastly
increased levels of enzymes associated with fat metabolism — means that,
at any given exercise intensity, a trained individual has to rely less on gly-
cogen, thereby ‘sparing’ their glycogen stores. This process is referred to as
glycogen sparing. Basically this means that glycogen stores are not utilised
as early in an exercise bout, subsequently delaying depletion of these stores,
and thereby delaying the time to exhaustion due to glycogen depletion.

Decreased utilisation of the anaerobic glycolysis

(lactic acid) system
The enhanced capacity of the muscles to aerobically metabolise glucose
and fats and other muscular level adaptations also means that there is
less reliance upon the anaerobic glycolysis (lactic acid) system to produce

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 energy for ATP resynthesis until higher exercise intensities are reached.
From a performance perspective, this allows the athlete to work at higher
exercise intensities without exceeding their lactate threshold. Or to put in
another way, aerobic training results in an increase in the lactate threshold
(for example, an athlete must run at a faster pace in order to accumulate
the same amount of blood lactic acid as before training).

Muscle-fibre type adaptation

Currently, there is some evidence to show that skeletal muscle switches fibre
types from fast twitch to slow twitch as a result of endurance training. Some
researchers have demonstrated a fast-to-slow fibre transformation in human
studies. Remember, on the basis of various structural and functional charac-
teristics, skeletal muscle fibres are classified into three types:
• Type 1 slow-twitch oxidative fibres
• Type 2A fast-twitch oxidative fibres
• Type 2B fast-twitch glycolytic fibres.

Figure 8.9:
Summary of muscle tissue Before training After training
adaptations to aerobic
(endurance) training Mitochondria
(size and Increased
number)

Glycogen
Increased
stores

Myoglobin Increased

Tryglyceride
stores Increased

Oxidation (both glucose and fat)

CHO fats
CO2+H2 Increased
O2 ATP

ADP + P

Anaerobic glycosis (lactic acid sytem)

ADP + P
Decreased
Lactic
CHO
acid

ATP

Muscle type adaptation Increased

Number
Some conversion of
Type 2B fibres to
Type Type 2A fibres

Key Type 2A fast-twitch

Type 2B fast-twitch

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 Type 1 fibres contain large amounts of myoglobin, and large numbers of
mitochondria and blood capillaries. Type 1 fibres are red, split ATP at a slow
rate, have a slow contraction velocity, are very resistant to fatigue, and have
a high capacity to generate ATP by oxidative metabolic processes.
Type 2A fibres contain an extremely large amount of myoglobin, and huge
numbers of mitochondria and blood capillaries. Type 2A fibres are red,
have a very high capacity for generating ATP by oxidative metabolic
processes, split ATP at a very rapid rate, have a fast contraction velocity, and
are resistant to fatigue.
Type 2B fibres contain a low myoglobin content, relatively few
mitochondria and blood capillaries, and large amounts of glycogen.
Type 2B fibres are white, are geared to generate ATP by anaerobic metabolic
processes, fatigue easily, split ATP at a fast rate, and have a fast contrac-
tion velocity. Individual muscles are a mixture of the three types of muscle
fibres but their proportions vary depending on the action of the muscle
and the genetic make-up of the individual.
There is now decent evidence to show that pure Type 2B fast-twitch
glycolytic fibres can make a transition to ‘hybrid’ Type 2A fast-twitch
oxidative fibres with chronic endurance training. The transformed
muscle fibres show a slight increase in diameter, mitochondria and
capillaries. This transformation is very gradual and can take years of
training to manifest itself. However, there is still some scientific argu-
ment about this process. Other researchers argue that it may well be that
Type 2B fast-twitch glycolytic fibres show an enhancement of their
oxidative capacity after high-intensity endurance training. This brings
them to a level at which they are able to perform oxidative metabolism as
effectively as the Type 1 slow-twitch fibres of untrained subjects. This is
brought about by an increase in mitochondrial size and number, and associ-
ated related changes, but not a change in fibre type per se.

Chronic adaptations to anaerobic training

Figure 8.10:
Anaerobic training effects are best developed through sprint training,
This body builder’s chronic shorter and faster interval training, plyometric training, circuit training, and
responses to anaerobic training resistance (strength and power) training. The greatest adaptations occur at
have led to muscle the muscle-tissue level. They include:
hypertrophy and an increase • muscle hypertrophy
in physical performance. • increased muscular stores of ATP and PC
• increased glycolytic capacity
• cardiac hypertrophy
• other anaerobic training adaptions.

Muscle hypertrophy
Anaerobic training can result in significant enlarge-
ment of muscle fibres (mainly Type 2B fast-twitch fibres)
resulting in muscular hypertrophy (an increase in the
cross-sectional size of the muscle) and subsequently,
greater strength, (figure 8.10). This hypertrophy occurs
as a result of an increased size and number of myofibrils
per muscle fibre and increased amounts of myosin and
actin myofilaments. Muscular hypertrophy is more pro-
nounced in males than females due to greater levels of
testosterone within men.

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 100
 


 

 Increased muscular stores of ATP and PC
90 Muscular hypertrophy is accompanied by increased muscular stores of ATP
80 and PC, as well as the enzymes required to break down and resynthesise

Adenosine triphosphate stores

70 ATP. This results in an increased capacity of the ATP–PC system, namely
60 greater energy release and faster restoration of ATP (figure 8.11). This ben-

Phosphocreatine stores
Creatine kinase activity

efits the athlete in activities that require speed, strength and power.
50

Glycolytic capacity
40 Increased glycolytic capacity
30
Enhanced muscular storage of glycogen and increases in the levels of gly-
20 colytic enzymes are also adaptations accompanying anaerobic training.
10 Consequently, the capacity of the anaerobic glycolysis (lactic acid) system to
0 produce energy is enhanced (figure 8.11).
Figure 8.11: Cardiac hypertrophy
Effects of anaerobic training
on muscular stores of ATP,
The most significant circulatory system adaptation resulting from anaer-
PC and glycogen
obic training is cardiac hypertrophy. Sustained anaerobic training results in
the hypertrophy (enlargement) of the heart muscle itself. However, rather
than increasing the size, and therefore volume, of the ventricular chambers,
which occurs after prolonged aerobic training, anaerobic training produces
an increase in the thickness of the ventricular walls (figure 8.12). While no
change in stroke volume occurs, a more forceful contraction takes place and
hence a more forceful ejection of blood from the heart.

(a) Untrained individual (b) Anaerobically trained athlete

Figure 8.12 (a) and (b):

Effects of anaerobic training
on cardiac hypertrophy.
Following intense sustained
anaerobic training, the thickness
of the ventricular wall increases,
particularly in the left ventricle,
but there is no increase in the Note: Thickening of wall
volume of the ventricular cavity. of left ventricle

Other anaerobic training adaptations

Other adaptations that take place during anaerobic training programs
include:
• an increase in the strength and size of connective tissues such as tendons
and ligaments
• an increase in the number of motor units recruited for maximum
contractions
• an increase in the speed of nerve-impulse transmission to the muscle cells
• an increase in the speed of muscular contraction.

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 Summary of chronic adaptations
to training
Table 8.1 summarises the chronic physiological adaptations resulting from
both aerobic- and anaerobic-type training programs.

Table 8.1
Summary of chronic training adaptations
Evident at:
Sub-
Tissue or maximal Maximal
system level Specific adaptation to types of training Rest exercise exercise
Circulatory system Aerobic training
Cardiac hypertrophy — increase in size Yes Yes Yes
(volume) of ventricular cavities
Increased capillarisation of the heart muscle Yes Yes Yes
Increased stroke volume Yes Yes Yes
Lower resting heart rate Yes NA NA
Lower heart rate during sub-maximal NA Yes NA
workloads
Improved heart-rate recovery rates NA Yes Yes
Increased cardiac output at maximum NA NA Yes
workloads
Lower blood pressure Yes Yes Yes
Increased a-VO2 diff Yes Yes Yes
Increased capillarisation of skeletal muscle Yes Yes Yes
Changes to blood cholesterol, triglycerides, Yes Yes Yes
low and high-density lipoprotein levels
Anaerobic training
Cardiac hypertrophy — increase in the Yes Yes Yes
thickness of the ventricular walls
Respiratory system Aerobic training
Increased lung ventilation Yes Yes Yes
Increased VO2 max NA NA Yes
Increased lactate threshold NA NA Yes
Muscle tissue Aerobic training
Increased oxygen utilisation No Yes Yes
Increased size of mitochondria Yes Yes Yes
Increased myoglobin stores Yes Yes Yes
Increased muscular fuel stores: Yes Yes Yes
Glycocen Yes Yes Yes
Triglycerides Yes Yes Yes
Free fatty acids Yes Yes Yes
Oxidative enzymes Yes Yes Yes
NA: not applicable

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 Table 8.1 (continued)
Summary of chronic training adaptations
Evident at:
Sub-
Tissue or maximal Maximal
system level Specific adaptation to types of training Rest exercise exercise
Muscle tissue Aerobic training (continued)
Increased oxidation of fats No Yes Yes
Decreased utilisation of the anaerobic glycolysis NA Yes Yes
(lactic acid) system
Muscle-fibre type adaptations Yes Yes Yes
Anaerobic training
Muscular hypertrophy Yes Yes Yes
Increased number of myofibrils Yes Yes Yes
Increased size of myofibrils Yes Yes Yes
Increased amounts of myosin and actin Yes Yes Yes
myofilaments
Increased capacity of the ATP–PC system NA NA Yes
Increased stores of ATP Yes Yes Yes
Increased stores of PC Yes Yes Yes
Increased glycolytic capacity NA Yes Yes
Increased storage of glycogen Yes Yes Yes
Increased levels of glycolytic enzymes Yes Yes Yes
Increased speed and force of contraction NA Yes Yes

Key knowledge Activity 3 Written report

• Chronic adaptations of
the cardiovascular, The ‘training effect’
respiratory and muscular
systems to training For this activity you are required to complete a written report
based on an investigation of the chronic adaptations to training
(the so-called ‘training effect’) typically experienced by an athlete
Key skill who participates in a prolonged training program for a specific sport.
• Summarise accurately
a Select a sport of your own choice.
information in relation to
b Consider an athlete at an elite level within this sport.
chronic adaptations to
c Investigate and briefly explain the main training methods that
training.
would be undertaken by an elite athlete in this sport.
d For each of the training methods you identify, outline all
the chronic muscular, cardiovascular and respiratory training
adaptations that could be expected after 12 months of training.
Also consider how these would benefit the performance of
the athlete in his/her specific sport.
e Provide supporting evidence for your discussion in the form
of data and findings from research studies, textbooks and
magazines.
f (Optional) Include pictures, diagrams and photographs to
support your discussion.
g (Optional) Present a summary of your findings to the rest of
the class.

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 Key knowledge Activity 4 Written report
• Chronic adaptations of
the cardiovascular, Chronic adaptations to a training program
respiratory and muscular
systems to training For this activity you are required to complete a written report
based on the results of your participation in a 6-week long ‘mini’
Key skill training program.
• Summarise accurately a Select a sport or physical activity of your own choice.
information in relation to b Determine the relevant fitness components and energy system
chronic adaptations to requirements of this sport or activity. (This might be based on
training. data you have collected previously when undertaking an activity
analysis.)
c Undertake a fitness assessment to determine your pre-training
fitness status.
d Design a 6-week long training program based on your activity
analysis and pre-fitness test results. Ensure that you adhere to all
training principles including frequency, intensity and progressive
overload.
e Undertake your 6-week training program.
f At the completion of your 6-week training program, undertake a
post-training fitness assessment.
g Present the results of your pre- and post-fitness test results using
appropriate tables and graphs.
h Discuss these results in groups
or as a class, drawing
upon your knowledge and
understanding of chronic
adaptations to training.
Include evidence to support
your findings and
conclusions.
i As a summary,
indicate how your
results might have
been further improved
or enhanced.

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 Key knowledge Chapter summary
• Chronic adaptations of
the cardiovascular, • Long-term responses that develop over a period of time (usually a
respiratory and muscular minimum of six weeks) when training is repeated regularly. These are
systems to training referred to as chronic adaptations to training. The combined effect of all
chronic adaptations is known as the training effect.
Key skill • Chronic adaptations to training may occur at both the tissue level —
• Summarise accurately within skeletal muscle fibres — and/or at the system level — particularly
information in relation to the cardiovascular and respiratory systems. The result of these physiolog-
chronic adaptations to ical adaptations is a significant improvement in performance.
training. • Chronic adaptations to training are dependent upon:

CHAPTER REVISION
— the type and method of training
— the frequency, duration and intensity of training
— the individual athlete’s capacities and genetic make-up.
• Table 8.1 (pages 262–3) summarises the main chronic training adaptations
that have been discussed in this chapter.

Review questions
1. Define in your own words the following key terms all of which appear in
this chapter. When you have finished, check your definitions with those
in the glossary on page 435.
Arterio-venous oxygen Capillarisation
difference (a-VO2 diff)
Cardiac hypertrophy Cardiac output
Chronic adaptations De-training
Glycogen sparing Hypertension
Lactate threshold Lung ventilation
Maximum oxygen uptake Mitochondria
(VO2 max)
Muscular hypertrophy Myoglobin
Oxidative enzymes Pulmonary diffusion
Respiratory frequency Stroke volume
Tidal volume Type 1 slow-twitch
oxidative fibres
Type 2A fast-twitch Type 2B fast-twitch
oxidative fibres glycolytic fibres
2. Which of the following is not a chronic adaptation to training?
(a) increased red blood-cell count
(b) increased capillarisation of the heart muscle
(c) increased muscular storage of glycogen
(d) increased resting heart rate.
3. Which of the following chronic adaptations to training would indicate
an improved level of aerobic fitness?
(a) decreased stroke volume at rest
(b) increased cardiac output during maximal exercise
(c) increased blood pressure at rest
(d) decreased arterio-venous oxygen difference during sub-maximal
exercise.

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 4. Outline and explain four chronic adaptations that may occur within
the circulatory system as a result of a long-term aerobic training
program.
5. (a) Outline five chronic adaptations that may occur at the muscular
level as a result of involvement in an anaerobic training program of
at least 12 weeks’ duration.
(b) Which adaptation is immediately evident in the athlete in
figure 8.13?
Figure 8.13:
Body builder in training
CHAPTER REVISION

6. Complete the following table by indicating in the blank spaces whether

the parameter is increased, decreased or unchanged as a result of
involvement in a long-term aerobic training program.
Table 8.2
Effects of aerobic training on muscle glycogen stores
Parameter At rest During sub-maximal During maximal
exercise exercise
Heart rate Decreased
Stroke volume Increased
Oxygen consumption Unchanged
Oxygen extraction
by muscles Unchanged
Lactic acid levels Decreased

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 35 7. Refer to figure 8.14. Which column (X or Y) indicates muscle glycogen
Y
stores after completion of a 20-week aerobic training program? Explain
30 your answer.
8. Outline two other changes that may occur within muscles as a result of


 



25

 

such an aerobic training program. How would these adaptations allow

20
an athlete to improve their aerobic performance?
9. Explain the likely differences in the hypertrophy of the heart that would
15 be experienced by an athlete who undergoes a 12-month aerobic
X
training program, as compared to an athlete who undergoes a 12-month
10 anaerobic training program. Use diagrams to assist your explanation.
10. Involvement in a long-term anaerobic training program (e.g.
5 sprint training) may result in an increase in an athlete’s lactate

CHAPTER REVISION
threshold. What chronic adaptations to training help bring about
0

 this improvement in an athlete’s lactate threshold? What advantages



 
  does a higher lactate threshold have for both anaerobic-type athletes

  (e.g. sprinters) and aerobic-type athletes (e.g. longer-distance
runners)?
Figure 8.14:
Effects of aerobic training on
muscle glycogen stores
Websites
www.atp4athletes.com/index.html Athletes Training for Performance
www.isokinetics.net/advanced/musclefibertypes.htm Isokinetics Explained
http://home.hia.no/~stephens Masters Athletes Physiology and
Performance (MAPP)
www.pponline.co.uk Peak Performance Online
www.brianmac.demon.co.uk/welcome.htm Sports Coach
www.teachpe.com Teach PE.com

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