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Exercise response in the presence of respiratory and cardiac diseases. Fang Lou. Learning Outcomes. By the end of this session and appropriate reading, successful students should be able to:. Describe the response to exercise in the presence of cardiac disease and respiratory disease
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Exercise response in the presence of respiratory and cardiac diseases Fang Lou
Learning Outcomes By the end of this session and appropriate reading, successful students should be able to: • 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
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
Who would benefit? • Traditionally available to post-MI and coronary artery bypass graft patients • Patients with angina • Chronic heart failure • Following angioplasty • Cardiac transplantation
Coronary artery disease (CAD) • 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)
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)
What are the benefits (2)? • 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
Oxygen uptake and VO2max • 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)
5 Fit 4 3 Unfit Oxygen uptake (VO2) (l/min) 2 1 MET 1 0 100 250 300 50 150 200 Work load (W) Work load against oxygen uptake Modified from Bethell,1996, Fig. 4.1
Heart rate against VO2 4 3 Fit 2 VO2 (l/min) Unfit 1 170 70 130 150 190 50 90 110 Heart rate Modified from Bethell,1996, Fig. 4.2
Fit 60 VO2 max (ml/min/kg) 50 Unfit 40 30 20 Before Training After Training Training effect in normal subjects VO2max aerobic capacity; starting point Modified from Bethell,1996, Fig. 5.1
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)
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
Heart rate against stroke volume 120 Normal S infarct 100 SV (ml) 80 60 120 M infarct L infarct 100 SV (ml) 80 60 70 90 110 130 150 170 70 90 110 130 150 170 Heart rate Heart rate Modified from Bethell,1996, Fig. 4.3
Effects of physical training on coronary patients • Effects are comparable with that of unfit subjects • Improvements in MI patients > healthy individuals(enhanced effect for programme started during natural recovery process) • Natural recovery: ~ 3 months after MI, physical work capacity and VO2max , marked by HR at given load, stroke volume • Remember FITT
Principle of exercise prescription • Frequency of training F • Intensity I • Duration / time T • Mode / type T
Optimal frequency range Increase VO2 max Orthopaedic complication 3 5 2 4 7 1 6 Time per week Exercise frequency Modified from Bethell,1996, Fig. 5.3
Optimal Intensity range Increase VO2 max Be aware of individual conditions! Risk of cardiac complications 70 50 85 100 % of max heart rate Exercise intensity Modified from Bethell,1996, Fig. 5.5
Optimal duration range Increase VO2 max Orthopaedic complication 20 40 30 10 Duration (min) Exercise duration Modified from Bethell,1996, Fig. 5.4
Recovery of SV with time after MI 100 75 The larger the infarct, the longer the recovery will continue SV at sub-max exercise (% of Normal) 50 25 1 2 3 4 Infarct Time (month) Modified from Bethell,1996, Fig. 5.2
Four stages for CR case • Phase I: in-hospital (average 5-7 days) • Phase II: immediate post-discharge (2-6 weeks) • Phase III: supervised outpatient exercise programme (6-12 weeks) • Phase IV: Long-term maintenance programme in the community
Exercise programme for MI patients • Phase I: in-hospital (5-7 days) • 2-3 times daily • rHR + 20-30bpm • 5-20 mins • Sitting/standing, walking • Phase II: immediate post-discharge (2-6 weeks) • 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
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)
Post-exercise hypotension Following exercise: • Resting blood pressure < baseline • Epinephrine, dopamine and cortisol • Sympathetic nerve activity • Secretion of endogenous opioids and serotonin
Hypertension • 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 • Mechanisms: primary and secondary • Factors contributing • Consequences if untreated (inc CAD) • Treatment (-blocker among the drugs, exercise)
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
Valsalva manoeuvre Contraction of abdominal & thoracic wall muscles; attempted expiration against a closed glottis Intrathoracic P, arterial P, small HR Vena cava being pressed, venous return, CO, arterial P, baroreceptor------tachycardia When the straining ends, intrathoracic P, arterial P, small HR Vena cava recovered, blood surges back to heart, CO, arterial P, bradycardia, then normal HR is good indicator, provided ANS is intact
Heart rate against VO2 vs.-blockade 4 3 VO2 (l/min) 2 With beta block Without beta block 1 70 130 150 50 90 110 Heart rate Modified from Bethell,1996, Fig. 5.7
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)
Long-term effects of exercise therapy • 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
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
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
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
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
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
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)
Nutrition (for your interest) • Food • Building blocks and repair • Form ATP • Pleasure • Nutrients: a substance in food that is used by the body to promote normal growth, maintenance, and repair • Essential nutrients: those molecules can not be made (converted from other molecules) by the body so must be provided by the diet
Major nutrients • Carbohydrates • Fat • Protein Minor (but equally crucial) • Vitamins • Minerals
The food guide pyramid Fats, oils and sweets use sparingly Meat, poultry, fish dry beans, eggs and nuts group, 2-3 servings Milk, yogurt and cheese 2-3 servings Vegetable group 3-5 servings Fruit group 2-4 servings Grain products 6-11 servings Modified from Marieb, Fig. 24.1
Serving size Grain products group • 1 slice bread • 0.5 cup cooked cereal, rice or pasta 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 For details, see McArdle 1999 Sports & exercise nutrition, p189
The calorie - a unit of food energy • 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 Modified from McArdle 1999 Sports & exercise nutrition, p166-7
Comparison of intake of middle-aged runnersand sedentary controls Runners % Seden.C. % Males Calories (kcal/day) 2959.0 2361.0 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 Females 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
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
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
Nutrition for exercise • 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
Effects of diet • 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
References • 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