1

Exercise response Exercise response in the presence of in the presence of

respiratory and cardiac respiratory and cardiac diseasesdiseases

Fang LouFang Lou

2

By the end of this session and appropriate reading, successful students should be able to:

Learning Outcomes

Describe the response to exercise in the presence of cardiac disease and respiratory disease

Explain the principle of exercise prescription in the presence of cardiac and respiratory disease

Appreciate basic concepts of nutrition and energy supply

3

Exercise training

Part of a rehabilitation programme

Focus on secondary prevention for MI

recovery; early stage benefit from low-

intensity aerobic exercise programme,

also facilitate both compliance and safety

Patients with chronic heart failure also

included

Effects lost on cessation of exercise

4

Who would benefit?

Traditionally available to post-MI and

coronary artery bypass graft patients

Patients with angina

Chronic heart failure

Following angioplasty

Cardiac transplantation

5

Central of the cardiovascular disease

A steady build-up of atherosclerotic plaques in the coronary arteries, leading to reduced blood flow

angina, arrhythmias (not totally blocked)

myocardium infarct (heart attack, totally blocked)

Prevention of CAD development

Rehabilitation of CAD patients (exercise therapy)

Coronary artery disease (CAD)

6

What are the benefits (1)?

Improvement in VO2max (peak performance)

Improving endurance (delay onset of fatigue)

Central: cardiovascular adaptation Increased left ventricular mass & chamber size

Increased total blood volume

Reduced TPR at maximal exercise

Peripheral: adaptive changes in the trained skeletal muscles (muscle oxidative capacity- extraction and utilisation of oxygen)

7

Exercise may have an important secondary

prevention role (risk factor modification):

A raised post-exercise metabolic rate

HDL (high-density-lipoprotein)

Improved insulin sensitivity

Decreased blood pressure

What are the benefits (2)?

8

VO2: rate of oxygen consumption

Metabolic equivalent (1 MET): the basal VO2 at

rest (3.5 ml/min/kg; ~250 ml/min in a standard 70kg man)

VO2max: The maximal rate at which an individual

can consume oxygen (normally 35-55 ml/min/kg (10-15 METs); ultra-fit athletes 70-80 ml/min/kg; cardiac patients much lower ~ 15-30 ml/min/kg)

Oxygen uptake and VO2max

9Modified from Bethell,1996, Fig. 4.1

Work load against oxygen uptakeO

xyg

en u

pta

ke (

VO

2)

(l/m

in)

1

2

3

4

50 100 150 200 250 300Work load (W)

5

0

Fit

Unfit

1 MET

10

UnfitVO

2 (

l/m

in)

1

2

3

4

50 70 90 110 130 150Heart rate

Modified from Bethell,1996, Fig. 4.2

Fit

Heart rate against VO2

170 190

11

VO2max aerobic capacity; starting point

Training effect in normal subjects

Modified from Bethell,1996, Fig. 5.1

VO

2 m

ax (

ml/m

in/k

g)

Before Training

AfterTraining

40

50

30

60

20

Unfit

Fit

12

Oxygen consumption by the myocardium

Factors contributing to VO2max: Heart rate Stroke volume Arterio-venous oxygen difference

Oxygen difference at rest: 70% in myocardium (very little to improve) 20% the rest of the body

The main factor to increase oxygen supply is to increase coronary blood flow (SV x HR)

13

Changes in SV for MI patients

Stroke Volume (SV) = EDV - ESV

Ejection Fraction (EF) = SV / EDV

In normal subject, EF > 60% at rest; it is much lower in patients with heart disease - as low as 10% in severe heart failure

During exercise, the increase in SV is greatly reduced with the increase in size of myocardial infarct, therefore increase in heart rate becomes the main factor

14

Heart rate against stroke volume

Normal

L infarctM infarct

S infarct

SV

(m

l)S

V (

ml)

120

120

100

100

80

60

60

80

90 11070 150 170130 90 11070 150 170130Heart rate Heart rate

Modified from Bethell,1996, Fig. 4.3

15

Effects of physical training on coronary patients

Natural recovery: ~ 3 months after MI, physical work capacity and VO2max , marked by HR at given load, stroke volume

Improvements in MI patients > healthy individuals (enhanced effect for programme started during natural recovery process)

Remember FITT

Effects are comparable with that of unfit subjects

16

Principle of exercise prescription

Frequency of training F

Intensity I

Duration / time T

Mode / type T

17Modified from Bethell,1996, Fig. 5.3

Exercise frequency

Time per week

Increase VO2 max

63 5 71 2 4

Orthopaediccomplication

Optimalfrequencyrange

18Modified from Bethell,1996, Fig. 5.5

Exercise intensity

Risk of cardiac complications

OptimalIntensityrangeIncrease

VO2 max

10070

% of max heart rate8550

Be aware of individual conditions!

19Modified from Bethell,1996, Fig. 5.4

Exercise duration

Optimaldurationrange

Orthopaediccomplication

Increase VO2 max

20 40Duration (min)

10 30

20Modified from Bethell,1996, Fig. 5.2

Recovery of SV with time after MIS

V a

t s

ub

-ma

x e

xerc

ise

(%

of

No

rmal

)

1 2 3 4

50

75

25

100

Time (month)Infarct

The larger the infarct, the longer the recovery will continue

21

Four stages for CR case

Phase II: immediate post-discharge (2-6 weeks)

Phase I: in-hospital (average 5-7 days)

Phase III: supervised outpatient exercise programme (6-12 weeks)

Phase IV: Long-term maintenance programme in the community

22

Exercise programme for MI patients

Phase II: immediate post-discharge (2-6 weeks)

Phase I: in-hospital (5-7 days) 2-3 times daily rHR + 20-30bpm 5-20 mins Sitting/standing, walking

Phase III: supervised outpatient exercise programme (6-12 weeks) 2-4 times weekly 60-75% MHR 20-30 mins Aerobic/endurance training involving large muscle

groups

23

Guideline of monitoring

Heart rate

Rating of perceived exertion

Metabolic cost (multiples of METs - metabolic equivalent )

ECG (for high-risk patients only)

(high-risk patients: functional capacity < 6 MET;

left ventricle ejection fraction <35%; exercise-induced hypotension)

24

Post-exercise hypotension

Following exercise:

Resting blood pressure < baseline

Epinephrine, dopamine and cortisol

Sympathetic nerve activity

Secretion of endogenous opioids and serotonin

25

Hypertension

Mechanisms: primary and secondary

Clinical intervention: For those not at high risk of CHD: SP>160, DP>90

Individuals with CHD/CVD: SP>140, DP>85

Diabetes: SP>130, DP>80

Factors contributing

Consequences if untreated (inc CAD)

Treatment (-blocker among the drugs, exercise)

26

Hypertension and exercise

Use FITT principles, but adopt lower intensity and longer duration

Adopt lower resistance/higher repetitions for resistance work; avoid high-intensity arm work and overgripping of equipment (e.g. cycle handlebars)

Avoid Valsalva manoeuvre

Warm-up is very important (acute BP is dangerous)

Consider drug side effects

27

Valsalva manoeuvre

Contraction of abdominal & thoracic wall muscles; attempted expiration against a closed glottis

1. Intrathoracic P, arterial P, small HR2. Vena cava being pressed, venous return, CO,

arterial P, baroreceptor------tachycardia

3. When the straining ends, intrathoracic P, arterial P, small HR

4. Vena cava recovered, blood surges back to heart, CO, arterial P, bradycardia, then normal

HR is good indicator, provided ANS is intact

28

With

bet

a blo

ck

VO

2 (

l/m

in)

1

2

3

4

50 70 90 110 130 150Heart rate

Modified from Bethell,1996, Fig. 5.7

Without b

eta block

Heart rate against VO2 vs. -blockade

29

Effect of -blockade on responses to exercise

Basic effects of -blockers: Heart rate and force Blood pressure In susceptible individuals, may precipitate asthma

Response to exercise: BP ; HR ; VO2max The linear relationship between % of VO2max and % of

MHR is unchanged Exercise alone can SP & DP by 10-20 mmHg

(intensity related, overtraining resting BP) Difficult to calculate MHR (has to be tested)

30

Sense of well-being (confidence) Anxiety and depression Exercise capacity ST segment depression on the ECG Blood pressure at rest Heart rate at rest Levels of serum cholesterol and triglycerides Elevated levels of HDL Perhaps mortality

Long-term effects of exercise therapy

31

COPD

Leg fatigue & muscle weakness

Caused by metabolic abnormality or

inactivity?

Reduction in cross-sectional area

Marked decrease in type I (endurance) and

type IIb (maximum strength) muscle fibres

Increased in endurance fibres of respiratory

accessory muscles

32

Pulmonary rehabilitation

Recognised long time ago (1895) that

exercise to be beneficial in the management

of respiratory disorder – dyspnoea in COPD

Multidisciplinary intervention including

physiotherapist

Aim at reducing the work of breathing and

improving disability

To aid the removal of secretions

Assessment of patient is important

33

COPD

Predominant symptom in COPD (Chronic

Obstructive Pulmonary Disease) is dyspnoea

Increased resistance in the airway

Associated with anxiety and fear

Patients report significant limitation in daily life

Previous experience could help reduce the

symptom

34

COPD

Is a disease with systemic effects

Muscle function further impaired by systemic

inflammatory agents

Peripheral muscle in COPD respond to

training in a similar manner to muscles in

healthy individuals

Other factors – nutritional status, hypoxia,

hypercapnia, inflammatory mediators,

circulating hormones – also contribute

35

Aims of pulmonary rehabilitation

Reduce dyspnoea

Increase muscle endurance

Improve muscle strength

Ensure long-term commitment to exercise

Help allay fear and anxiety

Increase knowledge of lung condition and

promote self-management

36

Exercise prescription

Same principle: FITT

Endurance or strength training?

40 to 60 min

Daily/x2 week/x3 week

Assessment

Symptom related (short of breath?)

Physiological test (VO2max)

Intensity (age and severity)

37

Nutrition (for your interest)

Nutrients: a substance in food that is used by the body to promote normal growth, maintenance, and repair

Food Building blocks and repair Form ATP Pleasure

Essential nutrients: those molecules can not be made (converted from other molecules) by the body so must be provided by the diet

38

Major nutrients

Carbohydrates

Fat

Protein

Vitamins

Minor (but equally crucial)

Minerals

39

The food guide pyramid

Fats, oils and sweetsuse sparingly

Milk, yogurt and cheese2-3 servings

Meat, poultry, fish dry beans, eggs and nuts group, 2-3 servings

Fruit group2-4 servings

Vegetable group3-5 servings

Grain products 6-11 servings

Modified from Marieb, Fig. 24.1

40

Serving sizeGrain products group

• 1 slice bread• 0.5 cup cooked cereal, rice or pasta

For details, see McArdle 1999 Sports & exercise nutrition, p189

Vegetable group• 1 cup raw leafy vegetable• 0.5 cup other vegetables cooked or chopped raw

Fruit group• 1 medium apple, banana, orange• 0.75 cup fruit juice

Milk group• 1 cup milk or yogurt• 2 oz processed cheese

Meat and beans group• 2-3 oz cooked lean meat, poultry or fish; • 0.5 cup cooked dry beans counts as 1 cup lean meat

41

One calorie: the quantity of heat to raise the temperature of 1 g (1mL) of water 1°C; kilocalorie (kcal) is used more

The joule (J) is the SI unit for energy; conversion of kcal to kJ: multiply the kcal value by 4.184

Calories contained in food: the potential energy trapped within the foods’ chemical structure; it can be measured in laboratory using a ‘bomb calorimeter’ (the heat liberated as food burns completely)

It depends on the structure of foods; average values: Carbohydrates: 4.2 kcal / g Lipids: 9.4 kcal / g Proteins: 5.65 kcal / g

The calorie - a unit of food energy

Modified from McArdle 1999 Sports & exercise nutrition, p166-7

42

Comparison of intake of middle-aged runners and sedentary controls

Males

Females

Runners %

Calories (kcal/day) 2959.0 2361.0

Seden.C. %

Proteins (g/day) 102.1 13.8 93.6 15.8

Lipids (g/day) 134.4 40.8 109.0 41.5

Carbohyd. (g/day) 294.6 39.8 225.7 38.6

Fat (g/1000 kcal) 25.2 25.3

Calories (kcal/day) 2386.0 1871.0

Proteins (g/day) 82.2 14.2 76.7 17.4

Lipids (g/day) 110.7 41.1 83.0 40.3

Carbohyd. (g/day) 234.3 39.5 174.7 39.1

Fat (g/1000 kcal) 25.3 24.4

Modified from McArdle Sports & exercise nutrition

43

Nutrition for exercise

Only carbohydrates, fat, and proteins can yield energy for muscular exercise. Protein is not used as a fuel as long as the energy supply is adequate.

The % of the two major fuels depends on, eg.:

Type of muscular exercise

State of physical training

The diet

State of health

44

Nutrition for exercise

At rest and during moderate exercise for a normal diet person, fats and carbohydrates contribute about equally

With increasing intensity of exercise, there is a gradual change toward a proportionally greater share of energy yield from carbohydrates (key point: oxygen supply)

Physical training can increase individual’s facility for fat utilisation

45

Type of performance (weight control for long-distance runners and high-jumpers)

Same proportion of fat intake for runner and weight lifter

Duration of performance Regular and well-balanced diet except the days proceeding

the event and the day itself

Events lasting less than 1hr: no special diet; no heavy meal; no meal <2.5hr before exercise

Events lasting between 1hr and 2 hrs: high-carbohydrate diet several days prior to exercise

Events lasting for several hours: same as above, plus ingestion of carbohydrates during the actual event

Nutrition for exercise

46

Effect of diet

47

Extreme high-fat diet (<5% from carbohydrates) for several days: duration of exercise is short (1hr); 70 to 99% use fat

Extreme high-carbohydrate diet (>90% from carbohydrates) for several days: duration of exercise is much longer (4hr); 20-30 to 60% use fat

Certain pathological conditions (diabetes) affecting the organism’s choice of fuel

Effects of diet

48

Bethell, H. (1996). Exercise-Based Cardiac Rehabilitation. Publishing Initiatives. Kent.

Brooks G.A., Fahey, T.D., White, T.P. & Baldwin, K.M. (2000). Exercise Physiology (Human Bioenergetics and Its Applications). 3rd ed. Mayfield Publishing Company. California.

Plowman, S. & Smith, D.L. (2003). Exercise Physiology. Benjamin Cummings. San Francisco

Pryor, JA & Prasad, SA (2002,) Physiotherapy for repiratory and cardiac problems. Churchill Livingstone.

Thompson, D. Bowman G.S., de Bono, D.P. & Hopkins, A. (1997). Cardiac Rehabilitation. Royal College of Physicians of London. London

References