Chronic adaptations to training - bss12pe

248LIVE IT UP 2

CHAPTER 8

Chronic adaptations to training

Whenever an individual engages in training there are two types of physiological responses that their body produces as a result of the demands of the exercise. These are:• Immediate, short-term responses that last only

for the duration of the training or exercise session and for a short time-period afterwards (recovery). These are commonly referred to as acute responses to exercise.

• Long-term responses that develop over a period of time (usually a minimum of six weeks) when training is repeated regularly. These responses involve the body adapting to the new demands

placed upon it and are referred to as chronic adaptations to training. The combined effect of all chronic adaptations is known as the training effect.This chapter examines the chronic adaptations to

training, that occur at the system (circulatory and res-piratory) level and the tissue (muscular) level.

Acute responses were covered in year 11 and are not directly assessed in the year 12 course. However, it may be useful to briefly revise these concepts as they provide a solid grounding for a complete under-standing of chronic adaptations (refer to chapters 5 and 6, Live it up 1, second edition).

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249CHAPTER 8 CHRONIC ADAPTATIONS TO TRAINING

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Assessment tasks

Task Topic Page

Data analysis exercise

Trained and untrained heart-rate responses (activity 1) 253

Case study analysis Lance Armstrong (activity 2) 255

Written reports The ‘training effect’ (activity 3)Chronic adaptations to a training program (activity 4)

263 264

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

After completing this chapter, students should be able to:

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250LIVE IT UP 2

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) trainingThe 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) trainingChronic 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.

Cardiovascular adaptations

Cardiac hypertrophy

Sustained aerobic training results in the enlargement of the heart muscle itself. This enlargement is referred to as cardiac hypertrophy. In endur-ance athletes, an increase in the size and therefore volume of the ventricular 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.

Figure 8.1 (a) and (b):

Effects of aerobic training

on cardiac hypertrophy

following intense, sustained

aerobic training. The size of the

ventricular cavities, particularly

the left ventricle, increases.


Capillarisation (blood supply) to

the heart before (a)

and after (b) a long-term

aerobic training program

(a) (b)

The two

coronary

arteries

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252LIVE IT UP 2

Increased stroke volume of the heart

The increased hypertrophy of the heart leads to a significant increase in the heart’s stroke volume. In other words, it ejects a greater volume of blood with each beat. Stroke volume is greater at rest, during sub-maximal exer-cise and during maximal workloads for a trained athlete, compared to an untrained person. For example, the average stroke volume at rest for an 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-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/beat (figure 8.3). Trained and untrained females have lower stroke volumes than their male counterparts under all exercise conditions, mainly due to their smaller heart size.

Lower resting heart rate

The amount of oxygen required by an individual while at rest basically does 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 × HRHowever, 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 × HR5 L/min = 70 mL/beat × 71 beats/min

After training:Q = SV × HR

5 L/min = 100 mL/beat × 50 beats/minIt 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 8.3:

Stroke volume in response to

aerobic training. Stroke volume

is greater for trained endurance

athletes at rest and at all

exercise intensities.

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RecoveryRest Moderatework

Key knowledge• Chronic adaptations of

the cardiovascular,

respiratory and muscular

systems to training

Key skill• Summarise accurately

information in relation to

chronic adaptations to

training.

Activity 1 Data analysis exercise

Trained and untrained heart-rate responses

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

minute 12 to minute 17?c Why does the heart rate remain above resting levels from

minute 18 to minute 26?d What are three physiological parameters that B has developed

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.

Increased cardiac output at maximum workloads

While cardiac output remains unchanged at rest and even during sub-maximal exercise regardless of training status, it does increase during 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 minute for untrained females.

By contrast, highly trained athletes have recorded values exceeding 30 litres per minute (figure 8.5).

Lower blood pressure

An aerobic training program may lower blood pressure, especially among people who suffer from hypertension (high blood pressure). Both systolic and diastolic pressure levels may decrease during both rest and exercise as a 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.

Figure 8.4:

Heart-rate responses before,

during and after sub-maximal

exercise for a trained athlete

and an untrained individual. Note

that the heart-rate response of a

trained endurance athlete (B)

is lower than that of an

untrained person (A) at rest

and at all exercise intensities.

The heart rate of a trained athlete

also returns to resting values

more quickly upon cessation

of exercise compared

with an untrained person.

Figure 8.5:

Cardiac output at rest

and at maximal exercise

for trained and untrained subjects

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254LIVE IT UP 2

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 lipoprotein (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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40 50 60 70mL/kg � min

40 50 60 70mL/kg � min

50.8

53.9

56.0

56.4

59.0

61.4

67.0

73.5

45.4

46.8

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51.5

62.1

Treadmill

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National-level Australian Footballers

Active young men

International-level soccer footballers

National-level volleyball players

National-level squash players

International-level field-hockey players

National-level middle-distance runners

National-level long-distance runners

Active young women

National-level volleyball players

National-level squash players

National-level field-hockey players

National-level middle-distance runners

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’.


the cardiovascular,


systems to training




training.

Activity 2 Case study analysis

Lance Armstrong

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

Lance Armstrong possess that enabled him to be so successful?b What other chronic training adaptations might Armstrong

have developed through training? List these under the following categories:• 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.

Figure 8.6:

Approximate maximum oxygen

uptake values of Australian

sportspeople

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256

LIVE IT UP 2

FUEL FOR

ARMSTRONG’S BODY

Professional cyclists such as Lance

Armstrong burn 4000 to 6000 calories

during a fl at stage and more than 8000

calories during a mountain stage.

Studies say the average human burns

between 1400 and 2500 calories a

day. All that energy has to come from

somewhere. Meals during the Tour

are simple and nourishing. Breakfast

consists of eggs, pasta, rice, bread,

yoghurt, cereals. During the race,

lunch is handed to the riders in bags

called musettes. They contain

high-carbohydrate items: small

sandwiches fi lled with honey and

banana slices, cakes, energy bars,

energy gells and water or sports drinks.

After a stage, team members snack on

cereal and high-protein foods. Dinner

consists of meats, pasta, rice, salad,

bread and dessert.

Tomorrow in Paris, Lance Armstrong

will call it quits. Barring an acci-

dent before the 2005 Tour de France

crosses the Champs Elysees fi nish

line, the 33-year-old American will

retire with a seventh straight yellow

jersey on his shoulders and a repu-

tation as one of the greatest athletes

of his generation.

Watching the devastating ease with

which Armstrong this week matched

every attack by his rivals in the steep

climbs of the Pyrenees, you would

think he was superhuman — and you

would be right. Armstrong is a physi-

cal freak, spectacularly well adapted

to the harsh demands of endurance

bicycle racing.

His heart is a third bigger than

average, pumping blood to his

muscles more effi ciently; at rest his

heart rate is 32 beats a minute, less

than half the average. His blood is

more saturated than normal, even for

a top-level sportsman, with energy-

producing oxygen; his VO2 max

rating, which measures how much

oxygen the lungs can consume during

exercise, is 85. An average healthy

male might rate a 40.

Even in an untrained state,

Armstrong is at the same level as a

highly trained but less gifted athlete,

according to scientist Edward Coyle.

Go back to those Pyrenean climbs

again. Armstrong can ride uphill

generating about 500 watts of power

for 20 minutes, something a typical

25-year-old could do for only 30

seconds. A professional hockey player

— perhaps even an AFL footballer —

might last three minutes then throw

up, according to Coyle, director of the

human performance laboratory at the

University of Texas.

Between 1992 and 1999 Coyle

had the unique opportunity to test

Armstrong’s body and chart how

it adapted to intense training and

competition. Armstrong was an

extraordinary athlete who … dra-

matically improved over time.

To do well, Coyle said, cyclists

needed a big heart, low levels of

lactic acid in their blood — the by-

product of intense exercise — and the

ability to effi ciently generate power,

measured as watts. When Armstrong,

then 20, fi rst asked Coyle for an analy-

sis of his potential, he already had the

big heart and low lactic acid. But his

muscle effi ciency was not very good,

Coyle said. It came in at 21 per cent.

That fi rst year, two other athletes

we studied were better. Armstrong

improved until his career was sus-

pended in 1996: he was diagnosed

with testicular cancer, which had

spread to his lungs and brain. Eight

months after his treatment ended,

Coyle’s tests found nothing perma-

nently wrong with Armstrong.

The last test was done in 1999,

after Armstrong won his fi rst Tour de

France.

In the previous two years his

lactic acid had dropped further and

his effi ciency increased to 23 per cent.

Together with the weight loss during

cancer treatment he was delivering

18 per cent more power — meaning

he could go faster up mountains with

less effort.

Coyle’s study, Improved Muscu-

lar Effi ciency Displayed as Tour de

France Champion Matures, in the

June issue of the Journal of Applied

Physiology, reveals the combination of

natural gifts and focused hard work

that took Armstrong to the top.

Stimulated by years of training

intensely for up to six hours most

days, Armstrong’s muscles changed

from 60 per cent slow-twitch fi bre —

the kind that doesn’t burn out quickly

— to 80 per cent.

Clearly, this champion embodies a

phenomenon of both genetic natural

selection and the extreme to which the

human can adapt to endurance train-

ing performed for a decade or more in

a person who is truly inspired, Coyle

wrote.

Good genes and sheer hard work.

Armstrong is a driven personality,

whose attention to detail shocked

the Europeans. Never had anyone

reconnoitred every mountain climb

months ahead of the tour — ridden

them repeatedly for training, as well

as memorised those parts where he or

other riders might attack.

Few, if any, top cyclists have

combined a precision diet to give

themselves exactly the right race-

ready weight in July with carefully

calibrated training and racing to

Lance Amstrong heads for triumph in the Tour de FranceBy Mike Van Niekerk

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MARATHON MANHEART & LUNGSA third larger than an average man’s, Armstrong’s heart has a resting

rate of an astounding 32 beats a minute. At peak exertion, it can race

up to 200 beats a minute. The average human’s resting heart beats 60

to 80 times a minute. The resting heart rate is the minimum number of

beats a minute needed to sustain the body.

• LUNGS The average healthy male’s lung capacity uses

40 millilitres of oxygen per kilogram of body weight

during exercise. Armstrong’s capacity is around 85.

STOMACHTeammates are responsible for bringing

Armstrong food during the race. Without it,

his body would run out of glycogen — the

short-term supply of carbohydrates stored

in muscles.

MUSCLES & BONESA product of metabolism, lactic acid

produces the excruciating burning

sensation familiar to participants in

strenuous physical activity. It could

be a side effect of his gruelling

training regimen or the

abnormally high percentage of

slow-twitch muscles in his body.

Armstrong produces less lactic

acid than normal.

• THIGH BONE Unusually long,

it allows Armstrong to apply

more force to the pedals.

• BODY FAT At about 4

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

fi rst week of the tour, when the race

hits the fi rst mountains. Jan Ullrich,

Armstrong’s most noted challenger

for six of the past seven years, is

well known to put on weight in the

off season then over-compensate by

losing the excess too quickly before

the tour, stressing his system.

Armstrong has surrounded himself

with experts, such as celebrity coach

Chris Carmichael and Italian Michele

Ferrari — although less openly since

he was implicated in a drugs scandal

— with whom he daily discusses

training statistics.

Finally, there is Armstrong’s

incredible desire to win. Even sur-

rounded by attacking rivals, as he has

been in this tour, he has never once sat

back when the challenges came.

It’s possible the 102-year-old Tour

de France will never again produce

another rider who can win seven

times straight. No one has done it

before.

Astonishingly, Armstrong has quit

at the height of his powers. It’s com-

monly accepted that on the strength

of this year’s performance, measured

against his rivals, he could likely win

an eighth yellow jersey in 2006.

What he’ll do now is open to spec-

ulation. Having earned a reported

$36.6 million in 2004 in salary and

endorsements, on top of previous

years’ earnings and with an ongoing

commercial relationship with the Dis-

covery Channel and other sponsors,

he’ll be able to do as he pleases. He

will certainly continue promoting

the work of his Lance Armstrong

Foundation for cancer research and

awareness.

In an interview with Outdoor mag-

azine last month, Armstrong said

that one night recently he drove with

his rock musician girlfriend Sheryl

Crow past the governor’s mansion in

his home town of Austin, the capital

of Texas. It’s a nice mansion. Nice

place, nice house, he teased. If he

does decide to go into public life, it’s

certain you will hear the name Lance

Armstrong in future just as often as

when he was winning the Tour de

France.

Source:

The Age, 23 July, 2005

Figure 8.7:

Case study of an elite athlete’s

adaptations to training

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258LIVE IT UP 2

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5 days perweek for28 weeks

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Figure 8.8:

Effects of aerobic training on

muscle tissue

Muscle tissue adaptations to aerobic (endurance) trainingChronic 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 8.9 opposite.

Increased oxygen utilisation

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

sites of ATP resynthesis (see chapter 2), and where glycogen and tri-glyceride stores are oxidised. The greater the number and size of the mitochondria located within the muscle, the greater the oxidisation of fuels to produce ATP.

• Increased myoglobin stores. Myoglobin is the substance in the muscle cell that attracts oxygen from the bloodstream into the muscle. Aerobic training significantly increases the myoglobin content in the muscle and therefore its ability to extract oxygen.

Figure 8.8 illustrates the effect of aerobic training on these parameters.

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

adaptations to aerobic

(endurance) training

Myoglobin

Increased

Increased

Increased

Increased

Increased

Decreased

Increased

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

Tryglyceridestores

Oxidation (both glucose and fat)

CHO fats

ADP + P

ATPCO2+H2O2

Anaerobic glycosis (lactic acid sytem)

ADP + P

ATP

CHOLacticacid

Glycogenstores

Before training After training

Mitochondria(size and number)

Muscle type adaptation

Number

Type

Key Type 2A fast-twitch

Type 2B fast-twitch

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260LIVE IT UP 2

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 trainingAnaerobic training effects are best developed through sprint training,

shorter and faster interval training, plyometric training, circuit training, and

resistance (strength and power) training. The greatest adaptations occur at

the muscle-tissue level. They include:

• muscle hypertrophy

• 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.

Figure 8.10:

This body builder’s chronic

responses to anaerobic training

have led to muscle

hypertrophy and an increase

in physical performance.

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0

20

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40

70

60

80

90

100� ��

Cre

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ina

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ctiv

ity

Ad

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osi

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tri

ph

osp

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te s

tore

s

Ph

osp

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atin

e s

tore

s

Gly

coly

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ap

aci

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Figure 8.11:

Effects of anaerobic training

on muscular stores of ATP,

PC and glycogen


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

volume of the ventricular cavity.

Increased muscular stores of ATP and PC

Muscular hypertrophy is accompanied by increased muscular stores of ATP and PC, as well as the enzymes required to break down and resynthesise ATP. This results in an increased capacity of the ATP–PC system, namely greater energy release and faster restoration of ATP (figure 8.11). This ben-efits the athlete in activities that require speed, strength and power.

Increased glycolytic capacity

Enhanced muscular storage of glycogen and increases in the levels of gly-colytic enzymes are also adaptations accompanying anaerobic training. Consequently, the capacity of the anaerobic glycolysis (lactic acid) system to produce energy is enhanced (figure 8.11).

Cardiac hypertrophy

The most significant circulatory system adaptation resulting from anaer-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

Note: Thickening of wall

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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262LIVE IT UP 2

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

Summary of chronic training adaptations

Tissue or

system level Specific adaptation to types of training

Evident at:

Rest

Sub-

maximal

exercise

Maximal

exercise

Circulatory system Aerobic training

Cardiac hypertrophy — increase in size (volume) of ventricular cavities

Yes Yes Yes

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 workloads

NA Yes NA

Improved heart-rate recovery rates NA Yes Yes

Increased cardiac output at maximum workloads

NA NA Yes

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, low and high-density lipoprotein levels

Yes Yes Yes

Anaerobic training

Cardiac hypertrophy — increase in the thickness of the ventricular walls

Yes Yes Yes

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

Table 8.1

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Summary of chronic training adaptations

Tissue or

system level Specific adaptation to types of training

Evident at:

Rest

Sub-

maximal

exercise

Maximal

exercise

Muscle tissue Aerobic training (continued)

Increased oxidation of fats No Yes Yes

Decreased utilisation of the anaerobic glycolysis (lactic acid) system

NA Yes Yes

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 myofilaments

Yes Yes Yes

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

Table 8.1 (continued)


the cardiovascular,


systems to training




training.

Activity 3 Written report

The ‘training effect’

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 who participates in a prolonged training program for a specific sport.a Select a sport of your own choice.b Consider an athlete at an elite level within this sport.c Investigate and briefly explain the main training methods that

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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264LIVE IT UP 2


the cardiovascular,


systems to training




training.

Activity 4 Written report

Chronic adaptations to a training program

For this activity you are required to complete a written report based on the results of your participation in a 6-week long ‘mini’ training program.a Select a sport or physical activity of your own choice.b Determine the relevant fi tness components and energy system

requirements of this sport or activity. (This might be based on data you have collected previously when undertaking an activity analysis.)

c Undertake a fi tness assessment to determine your pre-training fi tness status.

d Design a 6-week long training program based on your activity analysis and pre-fi tness 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 fi tness assessment.g Present the results of your pre- and post-fi tness 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 fi ndings and conclusions.

i As a summary, indicate how your results might have been further improved or enhanced.

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Chapter summary

• Long-term responses that develop over a period of time (usually a minimum of six weeks) when training is repeated regularly. These are referred to as chronic adaptations to training. The combined effect of all chronic adaptations is known as the training effect.

• Chronic adaptations to training may occur at both the tissue level — within skeletal muscle fibres — and/or at the system level — particularly the cardiovascular and respiratory systems. The result of these physiolog-ical adaptations is a significant improvement in performance.

• Chronic adaptations to training are dependent upon:— 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.


the cardiovascular,


systems to training




training.

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266LIVE IT UP 2

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 fi ve 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

fi gure 8.13?

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.

Figure 8.13:

Body builder in training

Table 8.2

Effects of aerobic training on muscle glycogen stores

Parameter At rest During sub-maximal

exercise

During maximal

exercise

Heart rate Decreased

Stroke volume Increased

Oxygen consumption Unchanged

Oxygen extraction by muscles Unchanged

Lactic acid levels Decreased

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7. Refer to figure 8.14. Which column (X or Y) indicates muscle glycogen stores after completion of a 20-week aerobic training program? Explain your answer.

8. Outline two other changes that may occur within muscles as a result of such an aerobic training program. How would these adaptations allow an athlete to improve their aerobic performance?

9. Explain the likely differences in the hypertrophy of the heart that would be experienced by an athlete who undergoes a 12-month aerobic training program, as compared to an athlete who undergoes a 12-month anaerobic training program. Use diagrams to assist your explanation.

10. Involvement in a long-term anaerobic training program (e.g. sprint training) may result in an increase in an athlete’s lactate threshold. What chronic adaptations to training help bring about 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)?

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

5

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X

Y

Figure 8.14:

Effects of aerobic training on

muscle glycogen stores

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