acute responses to exercise our body systems

O2 deficit

Respiratory

system

Muscular

system

Cardiovascular

system

Rest Exercise Recovery

Anaerobic

Aerobic

Steady state

Acute responses of body systems

↑ ATP demand

↑ Fuel requirement ↑ O2 delivery ↑ Waste removal

EPOC

Acute responses to

exercise

Our body systems— demand versus delivery

Our energy requirements are increased during the transition from rest to exercise so as to meet the greater demand for power output during muscle contraction. This need is met by our body systems, which increase the delivery of oxygen and fuels to the working muscles for ATP resynthesis. We already know that ATP can be generated via either anaerobic (oxygen-independent) or aerobic (oxygen-dependent) processes. However, when thinking about the physiological changes that occur at the onset of exercise, it is also important to consider the effects of the predominant energy

Figure 6.1

Acute responses of the

body systems to exercise

121

VCEPE_CH06-1.indd 121VCEPE_CH06-1.indd 121 30/06/10 2:43 PM30/06/10 2:43 PM

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Figure 6.2

Our respiratory,

cardiovascular and

muscular systems respond

rapidly to changes in

energy demand

Table 6.1: Acute respiratory responses to exercise

Condition Breathing rate (breaths/min)

Tidal volume (L/breath)

Ventilation (L/min)

Rest 12 0.5 6

Moderate exercise 30 2.5 75

Intense exercise 50 3.0 150

The respiratory system—a breath of fresh air

122 Macmillan VCE Physical Education 2 (Units 3 & 4)

system on the demand for oxygen and fuels, as well as the accumulation of metabolic byproducts that result. The immediate changes that are observed in the respiratory, cardiovascular and muscular body systems are a coordinated response to meet the increased energy demand of physical work. These rapid alterations to exercise intensity and duration are known as the body’s acute response s. In contrast, chronic responses to exercise develop over an extended period of time to cope with an ongoing training stimulus.

Chapter 6 explains the coordinated role of the respiratory, cardiovascular and muscular systems during the acute transition from rest to exercise. An overview of how these systems adjust to accommodate the energy requirements of exercise is provided in relation to the concepts of oxygen defi cit, consumption and debt. This chapter also discusses the acute effects of altitude exposure on these body systems.

Respiration increases during exercise in proportion to the metabolic needs of the working muscles to enable the exchange of oxygen and carbon dioxide (CO 2 ) to take place in the lungs. There is a rapid increase in ventilation at the onset of exercise, which at lower intensities is due to a greater tidal volume and at higher intensities is associated with an additional increase in breathing rate. It may surprise you to learn that in some cases this increase can begin even before exercise starts, as shown in fi gure 6.3 . It is thought to be the result of a central neural command initiated by the respiratory control centre located in the brain. The response serves as a feed-forward signal to assist in meeting the future energy needs of muscle contraction.

Figure 6.3 also shows the more gradual rise in ventilation seen in the second phase of exercise that is controlled by arterial blood concentrations of hydrogen (H + ) and CO 2 . Receptors in different locations around the body sense increases in the level of these metabolites (byproducts of metabolism)

Ventilation: the exchange of

air between the lungs and the

environment to allow oxygen

to be exchanged for carbon

dioxide in the alveoli

Tidal volume: the total

volume of air moved in and out

of the lungs during inspiration

and expiration


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High

Moderate

LowP

ulm

on

ary

ven

tila

tio

n (

L/m

in)

Time (min)

0

20

40

60

80

100

120

140

–2 –1 0 1 2 3 4 5 6 7


123CHAPTER 6Acute responses to exercise

and, in turn, increase both the rate and depth of respiration. These metabolite changes occur when the rate of ATP resynthesis is increased so as to promote oxygen release from the blood for energy production in the muscle.

Sustained exercise also increases heat and metabolite production, alongside ATP and O2 requirements. As body temperature increases, particularly during exercise in a hot or humid environment for a prolonged duration, ventilation will drift upwards. This is refl ective of the rise in blood temperature and the associated effect on the respiratory control centre. At the end of exercise, respiratory recovery can last several minutes, suggesting that our breathing is controlled during this period by acid-base balance (pH), temperature and the need to use oxygen above resting levels to restore fuels and metabolise the byproducts of energy production.

Figure 6.3

The effect of exercise

intensity on ventilation

Can swimmers improve their performance by training respiratory muscles?

>>

Figure 6.4

Swimmers can improve

endurance through

targeted training

of their respiratory

muscles


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Researchers at the University at Buffalo in America have shown that swimmers can improve their swimming endurance and breathing capacity through targeted training of the respiratory muscles. Specifi c protocols were followed for 30 minutes per day, fi ve days a week, for four weeks. The results of this study support those from previous research into cyclists, rowers and runners. The fi ndings suggest that athletes in most sports could improve their performance by undergoing respiratory muscle training. It is also clear that the greater the stress on the respiratory system with this type of training, the larger the improvement in performance.

Training the breathing muscles to improve the performance of swimming muscles seems counterintuitive, but is logical physiologically.

Researchers believe the muscles involved in moving the body become fatigued when we tire. However, the increased workload placed on the breathing muscles is very important, particularly under water during prolonged or high-intensity exercise such as swimming. As shown by other studies, when breathing muscles become fatigued, the body switches to survival mode and ‘steals’ blood fl ow and oxygen away from the locomotor muscles, redirecting it to the respiratory muscles to enable breathing to continue. Deprived of oxygen and fuel, the locomotor muscles become fatigued. Increasing the strength and endurance of the respiratory muscles prevents their fatigue during sustained exercise, enabling athletes such as divers and swimmers to work for longer periods without tiring.

The response of the respiratory system will also vary with exercise intensity and duration, and the training status of the individual. Table 6.2 shows typical ventilation ranges from laboratory testing of untrained and trained individuals across varying relative exercise intensities. Maximal ventilation rates of 80 to 120 litres per minute is commonly reported for untrained individuals compared to up to 150 to 220 litres per minute for well-trained to elite athletes.

Table 6.2: Ventilation ranges for untrained and well-trained individuals across different relative exercise intensities

Ventilation (L/min) Exercise intensity (% VO2max)

0–25 25–50 50–75 75–100

Untrained 15–25 30–40 60–80 80–120

Well-trained 25–40 40–60 100–120 150–220

Assessment workout Data analysis

Ventilation ratesUse table 6.2 to complete the following tasks.

1 Using the data in table 6.2, graph the expected ventilation of both untrained and trained

athletes working at 25, 50, 75 and 100 per cent of VO2max.

2 Explain why a well-trained person would be expected to have greater ventilation (L/min)

for the same relative exercise intensity compared to an untrained person. (Hint: compare

differences in absolute workloads performed and relate that to their energy needs.)

3 Why do elite 100 metre sprint athletes ‘huff and puff’ at the end of their event when sprinting

relies predominantly on anaerobic metabolism?

4 Swimmers use hypoxic training methods to improve performance by increasing their

tolerance of high concentrations of CO2 and H+. What do these metabolites promote that is

benefi cial for ATP resynthesis?


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Harvard athletes have the biggest muscles on campus and their hearts are no exception, according to a recent study that tracked the heart development of Harvard football players and rowers.

The fi ndings, presented by researchers at Massachusetts General Hospital and Harvard University Health Services, suggested that aerobic and endurance training can cause the chambers of the heart to

enlarge, while short-burst activities can increase heart muscle mass by up to 12 percent.

Using ultrasound technology, researchers evaluated the heart structures of athletes belonging


The cardiovascular system— pump up the volume

The cardiovascular system is a primary regulator of oxygen and fuel delivery to all body cells. As we transition from rest to exercise, our demand for ATP resynthesis and energy production increases in association with the modality (type), intensity and duration of the exercise performed. Numerous changes in the cardiovascular system occur during dynamic exercise in order to meet the increased ATP and energy requirements. The components of the cardiovascular system that are responsible for these changes are

heart rate (HR) stroke volume (SV) cardiac output ( Q ̇ ) blood pressure (BP) blood fl ow.

Heart rate Heart rate (HR) is one of the simplest measures used to gauge cardiovascular function both at rest and during exercise. It has a strong relationship with exercise intensity, which is why it is used by athletes to set training loads and recovery sessions. Although HR is used effectively as a training device, it is affected by other variables including fatigue level, hydration status, ambient temperature, altitude and illness. Resting HR normally ranges between 60 to 80 beats per minute (bpm), with elite endurance athletes having heart rates as low as 28 to 40 bpm.

Training the heart

Athletes’ hearts bulk upStudy fi nds that endurance training enlarges athletes’ heart chambers

BY ARIANNA MARKEL, CONTRIBUTING WRITER

>>

Figure 6.5

New Zealand team pursuit

cyclists hold position on the

start line at the Olympic

Games


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Figure 6.6

An athlete’s heartRight

Ventricle

Left

Ventricle

Normal heart Athlete’s heart

Enlargement of heart

muscle/left ventricle


Source: Extract from A Markel (2007), ‘Athletes’ Hearts Bulk Up’, The Harvard Crimson, 7 March, <www.thecrimson.com/article/2007/3/7/athletes-hearts-bulk-up-harvard-athletes/>

to the Harvard football team as well as the men and women’s crew teams at the beginning of the study and reassessed them after a three month period of ‘fairly intense training,’ according to Research Fellow in Medicine Aaron L. Baggish, one of the study’s lead researchers.

‘There were changes in [the heart structure of] almost every athlete,’ said Baggish, a cardiologist at Massachusetts General Hospital.

But he also emphasized that one of the key results of the study is that ‘different types of training affect the heart in different ways.’

By the end of the fall season, many of the football players’ hearts had accumulated up to 12 percent more muscle mass due to a thickening of their heart walls. While the mass of the rowers’ hearts did not increase as signifi cantly, the chambers of their hearts increased in size.

The Harvard researchers attrib-uted the different forms of heart growth to the emphasis on endurance in the sport of crew as opposed to the short, but intense bursts of energy required in football.

The study is part of an ongoing effort by Baggish and his colleagues to better understand the effects of athletic activity on the heart. As Baggish noted, their initial data does not address the long term impacts of athletics on the heart.

Immediately before an exercise effort or race it is normal to experience an anticipatory rise in heart rate. This is due to the release of hormones such as epinephrine (that is, adrenaline) from the adrenal medulla, located on the top of the kidneys. As exercise intensity increases there is a proportional linear rise in HR that will continue until the intensity approaches a maximal effort. At this time HR will plateau, even though exercise intensity may be increasing. This is indicative of HR reaching a maximal range.

The highest value observed at the point of fatigue is referred to as maximal HR (HR max ) and is used to set an athlete’s training zones. Although most elite athletes calculate their HR training zones using the results of sports-specifi c laboratory testing, to determine HR max it is common for the average person to use the following formula:

HR max = 220 – age (years)

The basis of this equation is that HR max slowly but surely declines with age; in fact it is thought to decline by one beat per year after the age of 15 years.

It is important to note that this calculation is only an estimation of HR max and it will vary greatly in accuracy between individuals. Sports scientists


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Figure 6.8

The effect of endurance

training on sub-maximal

and maximal heart rate,

as measured in a cycling

VO2max test

80

100 150 200 250 300 350 400 450

100

120

140

160

180

200

Hea

rt r

ate

(bp

m)

Power (watts)

Pre-training

Post-training

Hea

rt r

ate

(bp

m)

Power (watts)

Oxygen uptake (L/min)

100

150

200

0

0 1 2 3 4

50 150 200 250


often observe vastly different HR max values for two people of the same age and fi tness. Caution does need to be taken when using an estimated HR max value to set training intensities as the potential for error is large and may result in the training intensity being overestimated or underestimated.

Figure 6.7 shows the relationship between HR and exercise intensity such that, as the exercise intensity or workload increases, there is a linear rise in heart rate to meet the greater energy demand placed on the working muscles.

The data in fi gure 6.8 is taken from a cycling VO 2max test conducted in the Exercise Research Australia sports science laboratory on a well-trained triathlete. The data shows the HR responses of the same athlete on two separate occasions, 12 weeks apart, before and after endurance training. The graph shows a reduction in absolute HR for the same exercise intensity after training across all workloads, including at the point of fatigue (VO2max).

Stroke volume Heart rate is not the only variable to increase in response to exercise intensity; the left ventricle will also eject a greater volume of blood with each beat to assist in meeting the increased energy demands. This is referred

Figure 6.7

The linear relationship

between heart rate and

exercise intensity

Source: adapted from PO Astrand et al. (2003), Textbook of Work Physiology, 4e, Human Kinetics, Illinois, p. 285


creo

Str

oke

vo

lum

e (m

L/b

eat)

Exercise intensity (% VO2max )

max

0

Rest 25 50 75 100

50

60

70

80

90

100

110

120

130

Untrained

Trained

Elite

0

80

100

120

140

160

180

200

60 110 160 210

Str

oke

vo

lum

e (m

L/b

eat)

Heart rate (bpm)


to as the stroke volume (SV) of the heart and is directly controlled during exercise by the following four factors:

the volume of venous blood returned to the heart the capacity of the ventricle to expand for maximal fi lling (distensibility) the capacity of the ventricle to contract for maximal ejection (contractility) the pressure the ventricles must contract against.

The fi rst two factors directly infl uence the fi lling capacity of the ventricle, whereas the last two factors govern the emptying capacity of the ventricle. Figure 6.9 shows the relationship between SV and exercise intensity. In an active, untrained individual, SV will increase from 60 to 70 mL per beat at rest to 110 to 130 mL per beat during maximal exercise; whereas, in well-trained to elite athletes, SV will increase from 80 to 110 mL per beat at rest to 160 to 200 mL per beat at maximal effort. It is easy to see on the graph that SV increases with exercise intensity, reaching maximal capacity between 40 to 60 per cent of VO 2max . After this intensity it quickly plateaus until the point of fatigue, which coincides with maximal exertion.

Stroke volume: the volume

of blood expelled from the left

ventricle with each heartbeat

In contrast, other research has reported increases in SV during graded exercise reaching maximal exertion. This relationship appears to be linked to the aerobic fi tness status of the individual, as can be seen in fi gure 6.10 . The graph shows no increase in SV above approximately 60 to 65 per cent HR max for the untrained university group, consistent with previous fi ndings. A small rise in SV was reported for the distance-running group when approaching

Figure 6.9

The relationship between

stroke volume and exercise

intensity as measured in a

running VO2max test

Figure 6.10


stroke volume and exercise

intensity for untrained

students, trained distance

runners and elite athletes

Source: adapted from JH Wilmore, DL Costill & WL Kenney (2008), Physiology of Sport and Exercise, Human Kinetics, Illinois, p. 164

Source: adapted from B Zhou et al. (2001) ‘Stroke volume does not plateau during graded exercise in elite male distance runners’, Medicine

and Science in Sports and Exercise, 33, 1849–54


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Untrained

Trained

Elite

0

5

10

15

20

25

30

35

120 140 160 180 200

Car

dia

c o

utp

ut

(mL/

bea

t)

Heart rate (bpm)


maximal effort. However, a striking fi nding was that the elite athlete group showed a progressive linear rise in SV with incremental exercise to maximal exertion. In summary, there is support to suggest that during incremental exercise the stroke volume of endurance-trained athletes increases progressively to maximum with no plateau. This may be due to training adaptations that result in superior ventricular fi lling capacity.

Cardiac output During exercise of different intensities, adjustments in SV and HR combine to provide greater cardiac output ( Q ̇ ) in order to meet the increased demand for blood fl ow to deliver oxygen and nutrients to the working muscles. Figure 6.11 displays the linear relationship between Q ̇ and graded exercise intensity that enables increased fuel and oxygen delivery for muscle contraction. At the start of exercise, increases in Q ̇ arise from a rapid rise in both SV and HR that, in untrained individuals, is maintained until an intensity of approximately 60 per cent of VO 2max . Beyond this intensity, it is HR rather than SV that serves to increase Q ̇ ; whereas in well-trained and elite endurance athletes, increases in SV are believed to have a greater infl uence on Q ̇ at high exercise intensities.

Cardiac output: the total

volume of blood pumped from

the heart per minute (L/min)

The following formula represents this relationship:

Q ̇ ( L / min ) = HR ( bpm ) × SV ( mL / beat )

As the equation shows, Q ̇ can be calculated by fi nding the product of HR and SV. Resting levels range from 4 to 6 L/min with a maximal cardiac output of up to 20 to 40 L/min observed during heavy exercise, according to the size of the person and their endurance-training background. Typical values for each component at rest and during exercise are shown in table 6.3 below.

Table 6.3: Typical resting and maximal exercise values for HR, SV and Q̇ for college-age untrained subjects and trained endurance athletes

Subject HR(bpm)

SV(mL/beat)

Q̇(L/min)

Rest

Untrained male 72 × 70 = 5.0

Untrained female 75 × 60 = 4.5

Figure 6.11


cardiac output and exercise

intensity for untrained

students, trained distance

runners and elite athletes

Source: adapted from B Zhou et al. (2001) ‘Stroke volume does not plateau during graded exercise in elite male distance runners’, Medicine

and Science in Sports and Exercise, 33, 1849–54

(continued)


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Subject HR(bpm)

SV(mL/beat)

Q̇(L/min)

Rest

Trained male 50 × 100 = 5.0

Trained female 55 × 80 = 4.4

Maximal exercise

Untrained male 200 × 110 = 22.0

Untrained female 200 × 90 = 18.0

Trained male 190 × 180 = 34.2

Trained female 190 × 125 = 23.8

Source: from SK Powers and ET Howley (1990), Exercise Physiology, WmC Brown Communications Inc, p. 182

Table 6.3: (Continued)

Assessment workout Summary

The relationship between heart rate, stroke volume and cardiac outputComplete the following table using the formula provided and include appropriate units.

HR

Unit: _______

SV

Unit: ________

Q̇

Unit: ________

100 90

58 4.00

206 95

185 35.0

Blood pressure Mean arterial blood pressure (that is, blood pressure ) increases immediately in the transition from rest to exercise. The extent of this increase depends on the exercise intensity. When we perform whole-body endurance activities, the rise in mean arterial pressure is primarily due to increases in systolic pressure with little change seen in diastolic measures. Systolic blood pressure (SBP) refers to the pressure exerted by the heart during left-ventricle contraction that results in blood being ejected from the left ventricle and delivered around the body. During maximal exercise this value may increase from a resting level of 120 to above 200 mmHg due to increases in cardiac output. Diastolic blood pressure (DBP) refers to the pressure exerted by the heart during relaxation that allows blood to fi ll its chambers (atrium and ventricle) in readiness for contraction. In a healthy individual this pressure will remain around 80 mmHg during exercise.

Figure 6.12 also shows clear differences in blood pressure responses to upper and lower body exercise. As you can see, upper body exercise results in

Systolic: the contraction or

pumping phase of the heart

Diastolic: the relaxation or

fi lling phase of the heart


creo

Blo

od

pre

ssu

re (

mm

Hg

)

% VO2max

Arms, systolic

Arms, diastolic

Legs, systolic

Legs, diastolic

250

030 50 70 90 110

70

90

110

130

150

170

190

210

230


a greater blood pressure response compared to lower body exercise performed at the same energy output. This is thought to be due to a combination of factors including smaller muscle mass and vasculature of the upper body and greater energy expenditure to stabilise the body when exercising with the arms. It may surprise you to know that the responses of blood pressure to resistance exercise are signifi cantly greater than those seen during dynamic or endurance activity. Measures can reach up to 480/350 mmHg (SBP/DBP) due to high internal pressures within the chest cavity that result from holding your breath while lifting, pushing or pulling a heavy weight. This is also known as the Valsalva manoeuvre and is considered dangerous as it causes blood pressure to rapidly increase to an extreme range.

Blood fl ow Did you know that blood fl ow during maximal exertion for a person of average fi tness is greater than the maximum fl ow of a kitchen tap? Immediately after the onset of exercise there is a redistribution of blood fl ow throughout the body to meet the energy demands of active muscle. Specifi cally, an increase in blood fl ow to the active muscles and a reduction in blood fl ow to the organs occurs to meet the greater oxygen and nutrient demands. Several mechanisms work together to redistribute blood fl ow during exercise. They achieve these changes by prompting vasodilation of blood vessels in regions requiring increased delivery of oxygen and nutrients and vasoconstriction of blood vessels in regions that do not. These rapid readjustments are determined by the exercise intensity and refl ect the importance of muscle tissue over other body systems when physically active. Figure 6.13 (overleaf) shows the changes in cardiac output that occur with exercise of different intensities as a relative (percentage) and absolute (L/min) measure. As the graph shows, approximately 15 to 20 per cent of total blood fl ow is directed to muscles at rest, with this increasing to 80 to 85 per cent during maximal intensity exercise to meet the higher oxygen and nutrient demand. Although a smaller percentage of total blood fl ow will be directed to the brain and cardiac muscle when the intensity of exercise increases (A), considerably larger volumes of blood are directed to these tissues (B) due to the increase in cardiac output that occurs during exercise.

Vasodilation: widening

(swelling) of the blood

vessels causing an increase in

blood fl ow

Vasoconstriction: narrowing (shrinking) of

the blood vessels causing a

decrease in blood fl ow

Source: PO Astrand et al. (1965), ‘Intraarterial blood pressure during exercise with different muscle groups’, Journal of Applied Physiology, 20,

pp. 253–6

Figure 6.12

Blood pressure responses

to upper- and lower-body

exercise (cycling) at the

same relative intensity

(%VO2max)


creo

0 0

5

10

15

20

25

30

35

Rest Light Moderate

ExerciseMaximal

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Rest Light Moderate

ExerciseMaximal

A B

% C

ard

iac

ou

tpu

t

Car

dia

c o

utp

ut

(L/m

in)

KeyKidneys, liver, stomach, intestine, etc.

Skin Muscle Heart Brain


As we have seen, exercise results in a redistribution of blood fl ow by the cardiovascular system away from vital organs to the active muscle tissue. The vasodilation of capillaries not only increases blood fl ow but also the surface area for gaseous exchange of O 2 and CO 2 , delivery of nutrients and removal of metabolic waste products. To achieve up to a 20-fold increase in oxygen uptake that is common in endurance athletes, our physiological response to exercise must extend beyond an increase in cardiac output. Due to increased muscle blood fl ow and enhanced local circulation our tissues are able to take up more oxygen per 100 mL of circulating blood. This value is known as the arterial-mixed venous oxygen difference (a– v ̄ O 2 diff) and it can expand up to at least three times that of resting values during exercise. An increase in either maximal cardiac output or a– v ̄ O 2 difference will lead to a greater maximal O 2 consumption, as described by the Fick equation below.

VO 2 ( mL / min ) = Q ̇ ( mL / min ) × a − v ̄ O 2 diff (mL)

Table 6.4: A comparison of VO2max values for male and femaleathletes

Sport Gender VO2max (mL/kg/min)

AFL M 55–65

Basketball M 48–65

F 45–60

Cycling M 60–85

F 45–75

Hockey M 45–65

F 40–60

Netball F 40–60

Rowing M 60–75

F 55–70

(continued)

Figure 6.13

The relative (A) and

absolute (B) distribution of

cardiac output at rest and

during exercise


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Sport Gender VO2max (mL/kg/min)

Rugby M 42–66

Soccer M 53–66

Triathlon M 65–80

F 60–70

Source: Data from Australian Sports Commission and Exercise Research Australia (ERA)

Table 6.4 (Continued)

The muscular system— faster, higher, stronger

The numerous functions of the muscular system are performed by only three different types of muscle: cardiac, smooth and skeletal. Here we focus on skeletal muscle and its relationship to movement and energy production. In order for movement to occur we require skeletal muscle to contract for force and power production. The intensity and duration of exercise will in turn determine the type of muscle fi bres recruited and the force and frequency of muscle contraction. A single human muscle contains fi bres that shorten at different speeds and produce varying amounts of force. The terminology ‘slow twitch’ and ‘fast twitch’ is commonly

Figure 6.14

An Ironman triathlete

prepares to be taken to

VO2max

Figure 6.15

A gymnast’s skeletal

muscles contract for force

and power production

Source: ERA sports science laboratory, www.exerciseresearch.com.au


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0

20

40

60

80

100

% To

tal m

usc

le

World-class

sprinter

Average

active

person

Middle-

distance

runner

World-class

marathon

runner

Extreme

endurance

athlete

Slow (Type I)

Fast (Type IIa)

Fast (Type IIb)


used to classify fi bres according to a number of characteristics. However, scientists tend to favour the use of the terms ‘Type I’ and ‘Type II’, with the latter divided into subcategories of ‘IIa’ and ‘IIb’. The average person has an equal proportion of types I and II muscle fi bres, whereas athletes tend to have a greater distribution of the fi bre type that is particular to their sport.

Type I fi bres are more effi cient at using oxygen to generate ATP for continuous exercise requiring muscle contractions to occur for an extended time. These fi bres fi re at a slower rate than Type II fi bres and have greater fatigue resistance, proving valuable to endurance performance in distance running, swimming and cycling. Type II fi bres are capable of greater force production and contract at a faster rate. This makes them advantageous for performance in strength, speed and power events. The mitochondria content and oxidative capacity are highest in Type I fi bres and lower in Type IIa and IIb fi bres respectively. The opposite is true when comparing glycolytic (anaerobic) capacity with Type II fi bres possessing an enhanced glycolytic enzyme activity and amount that serves to increase the rate of glycogen/glucose breakdown and ATP resynthesis.

Glycolytic enzymes: enzymes involved in glycolysis

(breakdown of glucose or

glycogen to pyruvate and lactic

acid) for ATP production (e.g.

phosphofructokinase)

Oxidative capacity: the

capacity to use oxygen

The transfer of O 2 within the muscle for aerobic metabolism is facilitated by a protein called myoglobin . At the onset of exercise, and as intensity increases, a drop in the cellular concentration of O 2 (<10 mmHg) encourages its release from myoglobin and facilitates its transfer to the mitochondria for ATP resynthesis. In addition to increased oxygen consumption (VO 2 ) exercise also brings about a greater need to break down muscular fuel stores such as ATP, CP, glycogen and triglycerides (see chapter 5).

Although training has been shown to improve physiological responses to exercise such as VO 2max and Q ̇ , these traits, along with others, are also infl uenced by genetics or heritability. Table 6.5 lists a number of traits associated with elite performance and provides an estimate of their heritability.

Myoglobin: the oxygen-

transporting protein of

muscle that resembles blood

haemoglobin in function

Figure 6.16

Muscle fi bre type

distribution specifi c to

exercise


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Figure 6.17

Type II muscle fi bres are

better at generating short

bursts of strength or speed


Table 6.5: Heritability estimates for some human performance traits

Trait Heritability (%)

Maximal oxygen uptake (VO2max) ~50

Cardiac output (Q̇) 42–46

Muscle fi bre-type proportions 40–50

Explosive muscle power 67

Table 6.6: Summary of the body systems’ acute responses to exercise

Body system Acute responses

Respiratory system • increased tidal volume

• increased respiratory rate

• increased ventilation

Cardiovascular system • increased heart rate

• increased stroke volume

• increased cardiac output

• increased systolic blood pressure

• redistribution of blood fl ow to

active muscles

• increased a–v̄ O2 difference

Muscular system • increased muscle recruitment

• increased fuel metabolism

• increased oxygen consumption

• increased production of metabolic

byproducts

• increased temperature

Acclimatisation: the ability

of the body to physiologically

adapt to a new environment,

such as high altitude, in order

to reduce the physical stress

placed on the body systems


creo

>>


Training at high altitude

primarily occur in the respiratory and cardiovascular systems to maintain homeostasis in the unusual environment. See table 6.7 for a summary of the acute and chronic responses to altitude.

An immediate response to altitude exposure is hyperventilation. The reduced arterial pressure of oxygen (PO2) is detected by receptors located in the aortic arch and carotid arteries above an altitude of ~2,000 m. As a consequence, ventilation is increased in an attempt to raise the oxygen (O2) levels back to baseline values. A consequence of increased ventilation

System Acute Chronic

Respiratory Hyperventilation

• Bodily fl uids become more alkaline due

to reduction in carbon dioxide (H2CO3)

with hyperventilation

Hyperventilation

• Excretion of base (HCO3–) via the kidneys and

concomitant reduction in alkaline reserve

Cardiovascular • Increase in sub-maximal heart rate

• Increase in sub-maximal cardiac output

• Stroke volume remains the same or

decreases slightly

• Maximum cardiac output remains the

same or decreases slightly

• Sub-maximal heart rate remains elevated

• Sub-maximal cardiac output falls to or below

sea-level values

• Stroke volume decreases

• Maximum cardiac output decreases

• Decreased plasma volume

• Increased hematocrit

• Increased hemoglobin concentration

• Increased total number of red blood cells

Muscular/local • Decrease in skin temperature

• Increased oxygen transport to the tissue

• Increased lactate production

• Possible increased reliance on glycogen

as a fuel source

• Possible increased capilarisation

• Increased mitochondrial density

• Increased aerobic enzymes

• Loss of muscle mass

Source: adapted from WD McArdle, FI Katch & VL Katch (2007) Exercise Physiology: Energy, Nutrition, and Human Performance, Lippincott, Williams & Wilkins, Philadelphia,

Table 24.1

Table 6.7: Acute and chronic responses to altitude

It is now common for many different types of athletes to spend time at high altitudes to promote the different physiological adaptations that arise from training in an environment that has a lower air density. Although the relative concentrations of oxygen (O 2 = ~21 per cent) and nitrogen (N 2 = ~79 per cent) do not change with altitude, the air is less dense or ‘thinner’ as altitude increases. This means that there is less O 2 in each breath taken.

There are immediate compensatory responses and chronic adaptations to altitude training (acclimatisation) that take days to months. The acute responses will

Figure 6.18

Chronic adaptations to

altitude training can

take days to months


creo

80

0 1000 2000 3000 4000 5000 6000 7000 8000 9000

75

70

65

60

55

50

45

40

35

30

25

20

15

10

5

0

Altitude (m)

% D

eclin

e in

VO

2max

fro

m s

ea le

vel


is an increase in expired carbon dioxide (CO2) making the blood more alkaline which is associated with altitude sickness. The air at altitude is also cooler and drier than at sea level leading to higher evaporation rates, particularly during respiration and exercise. Dry lips, mouth and throat are some of the side effects associated with a moderate degree of dehydration that occurs in this environment.

Cardiovascular changes occur in response to the reduced partial pressure of O2 (PO2) at altitude. Immediately following exposure to increased elevation there is an increase in submaximal exercise heart rate (HR) by up to 50% of the values observed at sea level. Cardiac output at rest and during sub maximal exercise also increases in order to provide the muscles with

adequate oxygen. Stroke volume (SV) remains relatively unchanged when at altitude but the reduced availability of oxygen at the same relative intensity results in a lower VO2max and exercise capacity. Interestingly, VO2 values may be slightly higher at a specifi c workload (power output or speed) when working at altitude due to a higher HR and relative exercise intensity.

Chronic responses are generally more desirable for physical performance and are related to additional hematological (blood) and local muscular adaptations. It is generally accepted that athletes need to exceed 2200 m for a period of 3–6 weeks in order to bring about optimal physiological adaptations that will result in enhanced performance.

Figure 6.19

The inverse

relationship between

VO2max and altitude

Source: adapted from WD McArdle, FI Katch & VL Katch (2007) Exercise Physiology: Energy, Nutrition,

and Human Performance, Lippincott, Williams & Wilkins, Philadelphia

Assessment workout Research task

Altitude sickness1 Complete the summary table below by identifying a mountain and country for each altitude

classifi cation.

Altitude classifi cation Height (m) Mountain Country

Near sea level 0–500

Low 500–2000

Moderate 2000–3000

High 3000–5500

Extreme >5500


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HOT questionsAcute responses of the body systems to exercise

KNOW 1 List the body systems that undergo rapid adjustments at the onset of

exercise and provide a brief summary of their role.

COMPREHEND 2 Explain how ventilation responds to increasing exercise intensity and

relate this to energy demand.

APPLY 3 What is the Fick principle and how does it relate to metabolism and

cardiovascular function?

ANALYSE

EVALUATE

CREATE

4 Discuss how heart rate, stroke volume and cardiac output respond to

increased exercise intensity. Graph each variable against relative exercise

intensity as % VO2max.

5 Discuss the acute effects of altitude on the body systems and compare

these to the effects of exercise performed at sea level. Include the

muscular system in your answer.


Oxygen consumption during exercise

Although an acute response to exercise is an increase in oxygen consumption to meet the ATP requirements, the aerobic system is unable to respond to these demands immediately due to a lag in the initiation of this system. We therefore need to rely on an alternative source for ATP resynthesis: the anaerobic energy systems.

The energy supplied from the anaerobic sources during this transition from rest to exercise is referred to as the oxygen defi cit . As exercise continues, we will either reach a steady state of O 2 consumption, using the contribution from the aerobic system, or continue to increase O 2 uptake and utilisation. At the end of exercise during recovery, O 2 consumption does not immediately decrease to a resting level. It is used for a number of processes, including the restoration of muscle fuels such as ATP, CP and glycogen, the metabolism of lactate and the replacement of oxygen to myoglobin.

Oxygen consumption: the

volume of oxygen used by

the body in a minute, usually

expressed in millilitres or litres

Oxygen defi cit: the energy

supplied by anaerobic sources

at the onset of exercise due

to the lag time of the aerobic

energy system

Steady state: the condition

of a system or physiological

function that remains at a

relatively constant (steady)

value; after a few minutes

of sub-maximal exercise, a

person will reach a steady

state in which heart rate and

oxygen consumption remain

constant for a given exercise

intensity

2 Research the following illnesses that are associated with exposure to altitude. Summarise

the possible causes, symptoms, treatment and prevention.

• acute mountain sickness

• cerebral oedema

• pulmonary oedema .


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A

B

Oxy

gen

co

nsu

mp

tio

n (

L/m

in)


Phase 1 Phase 2 Phase 3

O2deficit

VO2max

O2 requirement

EPOC

Oxy

gen

co

nsu

mp

tio

n (

L/m

in)


O2 uptake

O2 uptake

Phase 1 Phase 2 Phase 3

O2deficit

VO2max

Steady state

Low- to moderate-intensity exercise

Maximal intensity exercise

EPOC


What metabolic changes need to occur as a swimmer moves from a stationary position on the starting block to race pace in the pool to win an event? In the transition from rest to exercise, oxygen consumption rapidly increases in an attempt to meet the energy requirements of contracting muscle. Figure 6.20(A) shows a typical pattern of oxygen consumption from the onset of exercise to the achievement of steady state metabolism followed by the recovery phase after exercise. When we commence low to moderate

Figure 6.21

Oxygen consumption

rapidly increases in an

attempt to meet the energy

requirements of contracting

muscle

sub-maximal exercise, our oxygen consumption increases rapidly until it is able to meet the requirements of the exercise intensity (that is, steady state), which for most people will take between 2 and 3 minutes. During this time we rely heavily on the anaerobic contribution of ATP from the ATP-CP and lactic acid energy systems due to the inability of the aerobic system to resynthesise ATP at the required rate. This occurs through the breakdown of the fuels CP and muscle glycogen, producing the byproducts creatine and lactic acid.

The delay or lag in oxygen use is referred to as oxygen defi cit. This concept should be interpreted as the quantitative difference between the total amount of oxygen that would have been consumed if steady state was achieved immediately at the start of exercise and the amount of oxygen that actually

Phase 1: rest to exercise—oxygen defi cit

Figure 6.20

Oxygen consumption during

low- to moderate-intensity

exercise (A) and maximal-

intensity exercise (B)

Source: adapted from WD McArdle, FI Katch & VL Katch (2007) Exercise Physiology: Energy, Nutrition, and Human Performance, Lippincott,

Williams & Wilkins, Philadelphia


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was consumed during exercise. This is represented by the shaded area above the oxygen consumption (O2 uptake) curve in phase 1 of fi gure 6.20(A) .

Interestingly, research in this area has revealed that O 2 defi cit and anaerobic energy utilisation is not affected by the rate of transition from rest to exercise. Scientists from Sweden asked subjects to cycle for 10 minutes at 70 per cent VO 2max and either increased the workload from rest to exercise immediately or gradually over a 15-minute duration. They reported that the O 2 defi cit at the onset of exercise is not due to a delay in O 2 transport, but may be due to a limited utilisation of O 2 as a result of metabolic adjustments within muscle cells. Increases in ADP and P i are suggested to be primary metabolic regulators that activate both aerobic and anaerobic energy production resulting in the O 2 defi cit.

In aerobically trained athletes, oxygen defi cit is reduced due to these individuals reaching steady state more rapidly than an untrained person. Consequently, the total volume of oxygen consumed by endurance trained athletes is greater, most likely due to an enhanced ability to resynthesise ATP aerobically. This is brought about by specifi c endurance-training adaptations that optimise the function of the respiratory, cardiovascular and muscular systems. The factors that infl uence oxygen defi cit include:

exercise mode intensity and duration training status the muscle fi bre type recruited.

Athletes going into ‘defi cit’

Sprint-trained athletes routinely test their ability to generate energy anaerobically by performing anaerobic power and capacity tests in a sports science laboratory.

Elite 400 metre track sprinters will run on a treadmill at an intensity of 20 to 22 kilometres per hour at a 4 per cent gradient for as long as possible while measuring O 2 use from rest to fatigue.

These tests typically last between 60 and 120 seconds and are a useful tool for the sports scientist and coach to discuss an athlete’s ability to activate and sustain anaerobic ATP production to maximise muscle power and speed.

Figure 6.22

This runner

understands what it

feels like to perform at

maximal effort while in

oxygen defi cit


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Phase 2: sub-maximal exercise—steady state During steady state exercise of moderate duration, oxygen consumption will plateau, representing an equilibrium point in ATP supply and demand. In simple terms, this can be explained as an exercise intensity at which the aerobic system is able to meet the rate of ATP resynthesis required by the working muscles (that is, demand = supply). This is represented by the fl at portion on the graph in fi gure 6.20(A) (on page 139) and coincides with a plateau in ventilation, HR and blood lactate concentration. From steady state exercise, oxygen consumption can rise for a number of reasons, including an increase in intensity due to a greater demand for ATP (see fi gure 6.20 ). We will also see an upward drift in oxygen consumption if the environment is hot and/or humid or if the exercise intensity is maintained at a high relative work rate (>70 per cent VO 2max ) during prolonged exercise. A factor that would infl uence this response is training status, as a well-trained or elite athlete can reach a steady state at higher relative exercise intensities than an untrained person. Note that the factors mentioned above can be attributed to a rise in body temperature.

As shown in fi gure 6.20(B) , O 2 consumption will continue to rise with increased exercise intensity until VO 2max is reached. At this point, oxygen consumption cannot increase as the delivery and utilisation of O 2 by working muscles has reached a maximal level. However, a maximal value can be increased via physiological adaptations from training that enhance O 2 delivery and consumption.

Practical applicationUnderstanding oxygen defi cit

Step 1 Wearing a HR monitor, complete a 20-second maximal effort sprint (run or cycle) and record your HR at the end of the exercise. (Note: HR will continue to increase after exercise so make sure you read the monitor at exactly 20 seconds.)Recovery: Walk for 5 minutes before continuing with Step 2.

Step 2 Wearing a HR monitor, complete a 2-minute maximal effort (run or cycle) and record your HR at the end of the exercise.

Answer the following questions using your results.1 Which effort produced the highest HR value?2 Explain your answer to question 1 taking into account that the 20-second effort

was performed at a higher intensity. Refer to the concept of oxygen defi cit in your answer.

3 If you were an elite marathon runner how would oxygen defi cit and anaerobic ATP contribution be affected?

Figure 6.23

A marathon runner can

sustain steady state at

higher intensities than an

untrained person

Steady state exercise: an

intensity of exercise for which

ATP supply can adequately

meet ATP demand for a

moderate duration


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Figure 6.24

Athletes recovering after

their heat in a heptathlon


Phase 3: recovery—excess post-exercise oxygen consumption

At the completion of exercise why is it that we do not return to resting values immediately? Instead, we continue to breathe hard and sweat, with a heart rate that remains above resting levels. In the fi rst few minutes immediately after exercise our demand for energy decreases rapidly (exponentially) but still remains higher than baseline or resting levels.

The extent to which post-exercise oxygen uptake is elevated above resting values is termed excess post-exercise oxygen consumption ( EPOC ). EPOC was formerly referred to as oxygen debt , as it was believed that the oxygen ‘borrowed’ from the anaerobic system at the onset of exercise (oxygen defi cit) needed to be ‘paid back’ during recovery. This is a somewhat simplifi ed view of the EPOC–oxygen defi cit ratio . In fact, EPOC exceeds values for O 2 debt due to the additional physiological factors that need to return to baseline levels, as summarised in fi gure 6.25 . EPOC is affected by both exercise intensity, when it exceeds 50 per cent VO 2max , and duration.

Research has shown that exercise intensity is about fi ve times more important than either exercise duration or the combined effect of both intensity and duration in determining the magnitude of EPOC. A ‘rapid’ and ‘slow’ portion of EPOC is often referred to when discussing the function of oxygen consumption during the post-exercise recovery period. The ‘rapid’ portion of EPOC is normally associated with O 2 consumption immediately (about 3–5 minutes) after exercise has ceased. This period is believed to be responsible for the resynthesis of fuels such as CP and ATP, and restoration of O 2 stores to muscle and blood; whereas, the ‘slow’ portion of EPOC is associated with the oxidation of lactate, or its conversion to glycogen, and returning heart rate, respiration, body temperature, and hormone (epinephrine and norepinephrine) levels to baseline values. Table 6.8 reports values for O 2 defi cit and EPOC across different relative exercise intensities and durations.

EPOC: excess post-exercise

oxygen consumption above

resting levels during recovery

Oxygen debt: a term

formerly used to describe

oxygen consumption in the

period immediately after

exercise

EPOC–O2 defi cit ratio: the

relationship between the O 2

defi cit and the EPOC values for

a bout of exercise; the ratio

will generally be >1, as the

EPOC exceeds the O 2 defi cit


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EPOC

Rapid Slow

Resynthesis of fuels in muscle

Restoration ofmuscle and blood

oxygen stores

Resynthesis ofmuscle

glycogen

Elevatedhormones

Elevated HRand respiration

Elevated bodytemperature

Lactatemetabolism


Table 6.8 : Effect of exercise intensity and duration on O 2 defi cit and EPOC

Exercise intensity (VO2max)

20-min duration 50-min duration 80-min duration

O2 defi cit EPOC EPOC: O2 defi cit



30% x̄ 0.71 1.01 1.8 0.77 1.43 0.8 1.01 1.04 2.4

SD 0.33 2.76 3.8 0.34 2.84 7.0 0.56 3.01 8.6

50% x̄ 1.85 3.14 1.6 1.85 5.19 3.1 1.96 6.10 3.4

SD 0.39 3.58 2.0 0.49 3.83 2.5 0.48 4.22 2.6

70% x̄ 2.98 5.68 1.9 2.89 10.04 3.5 3.40 14.59 4.5

SD 0.60 4.89 1.6 0.48 3.26 1.3 0.86 2.94 1.2

* Means (x̄ ); standard deviations (SD)

Source: CJ Gore & RT Withers (1990), ‘The effect of exercise intensity and duration on the oxygen defi cit and excess post-exercise oxygen consumption’, European Journal of Applied

Physiology and Occupational Physiology, Springer-Verlag, 60, p. 171 Source: www.visualcoaching.com

Figure 6.25

Summary of rapid and slow

factors that infl uence EPOC


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HOT questions


Oxygen consumption, defi cit and EPOC

KNOW 1 Defi ne the terms oxygen defi cit and EPOC.

COMPREHEND 2 Explain why EPOC is greater following high-intensity exercise compared

to low-intensity exercise.

APPLY 3 How could a person reduce the oxygen defi cit component of exercise?

Explain your answer using your knowledge of body systems.

ANALYSE

EVALUATE

CREATE

4 On one graph, draw the oxygen consumption curves for an aerobically

trained and untrained person for exercise at 70 per cent VO2max.

Analyse the differences in oxygen defi cit and explain using correct

terminology.

5 Discuss how sports specifi c training would affect EPOC and compare

a sprint and endurance athlete in terms of post-exercise oxygen

requirements for fuel resynthesis and lactate metabolism.

Our energy requirements are increased during the transition from rest to exercise so as

to meet the greater demand placed on power output during muscular contraction. This

need is met by the rapid adjustments in body-system function that increase the delivery of

oxygen and fuels to the working muscles. These alterations in respiratory, cardiovascular

and muscular function as a result of changing intensity and duration are known as the acute

responses to exercise.

Exercise increases the demand for ATP resynthesis, which in turn promotes rapid adjustments

from our respiratory, cardiovascular and muscular body systems.

Ventilation increases in direct proportion to the energy requirements of the working muscles

and will be infl uenced by a person’s body size.

At lower exercise intensities increases in ventilation occur as a result of increases in tidal

volume.

At higher exercise intensities increases in ventilation occur as a result of increases in

breathing rate.

Maximal ventilation rates of 80 to 120 litres per minute is commonly reported for untrained

individuals compared to 150 to 220 litres per minute for well-trained to elite athletes.

Heart rate (HR) increases linearly with increased exercise intensity up to maximal effort

(VO2max).

CHAPTER SUMMARY


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Stroke volume (SV) also increases in proportion to exercise intensity, with maximal values

occurring in an untrained person at approximately 40 to 60 per cent VO2max.

Research has shown that SV in well-trained or elite athletes increases even up to maximal

intensity exercise to assist with delivery of oxygen and nutrients.

Increases in HR and SV combine during exercise to enhance cardiac output (Q̇) to meet the

greater energy needs of the working muscles and assist with removing waste products.

Mean arterial blood pressure increases in direct proportion to exercise intensity primarily

due to increases in systolic pressure.

Systolic blood pressure can exceed 200 mmHg during intense exercise as a result of

increases in cardiac output (Q̇).

Upper body exercise results in a greater rise in blood pressure compared to lower body

exercise at the same relative intensity.

Redistribution of blood fl ow occurs during exercise to minimise fl ow to the vital organs and

maximise fl ow to the working muscles.

The magnitude of a – v̄O2 difference also increases with exercise intensity due to greater

extraction of oxygen from the blood (arterial) by the active muscles.

When low to moderate sub-maximal exercise is performed, oxygen consumption increases

rapidly from resting levels until it is able to meet the requirements of exercise intensity. At

this point an athlete is said to be in steady state.

The delay in oxygen use to meet ATP demands during the transition from rest to exercise

results in a large amount of energy being supplied from anaerobic sources. This period of

time is referred to as oxygen defi cit.

In aerobically trained athletes, oxygen defi cit is reduced due to these individuals reaching

steady state more rapidly than an untrained person.

Factors that infl uence oxygen defi cit include exercise mode, intensity and duration, as well as

the training status of the person.

During steady state exercise of moderate duration, oxygen consumption will plateau,

representing an equilibrium point in ATP supply and demand.

Excess post-exercise oxygen consumption (EPOC) is affected by both exercise intensity

and duration.

The ‘rapid’ portion of EPOC (3–5 minute period) is normally associated with the resynthesis of

fuels such as CP and ATP, and restoration of O2 stores to muscle and blood.

The ‘slow’ portion of EPOC is associated with the oxidation of lactate and its conversion

to glycogen, as well as returning heart rate, respiration, body temperature, and hormone

(epinephrine and norepinephrine) levels to baseline values.


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acute responses to exercise our body systems

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