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EXERCISE AND THE CARDIOVASCULAR SYSTEM (CVS)

SECTION 1

1.1 Structure and function of the cardiovascular system The cardiovascular system consists of a double pump (the heart) and a system of blood vessels to transport the blood around the body. In the healthy individual, the cardiovascular system works very efficiently, but it is subject to several degenerative changes (some avoidable, some unavoidable) such as atherosclerosis, which may result in the development of cardiovascular disease (CVD) particularly coronary heart disease (CHD) which may ultimately result in a heart attack (myocardial infarction – MI). Before examining the pathophysiology of cardiovascular disease, we must understand the normal functioning of the cardiovascular system. Blood vessels There are three types of blood vessels within the cardiovascular system: • Arteries (and arterioles) carry blood away from the heart. The largest arteries (e.g. the aorta) have thick, elastic walls which can stretch to accommodate the surge of blood after each contraction of the heart. Arteries branch many times, forming smaller and smaller vessels, the smallest of which are arterioles. Contraction of the smooth muscle lining the walls of the arterioles allows them to open or close to varying degrees to adjust blood flow to different parts of the body. For example, when we are faced with danger, arterioles in the skeletal muscles dilate, which increases the blood flow (and therefore the oxygen supply), allowing us to flee or face the danger head on. (This is part of the ‘fight or flight’ response.) At the same time arterioles in the digestive system constrict, reducing blood flow to the gut and increasing the blood available to the muscles. • Capillaries are tiny vessels where the exchange of substances with the tissues occurs. Their walls are only one cell thick, allowing nutrients and waste to pass through with ease. They form extensive branching networks (capillary beds) throughout the body tissues, but only certain beds are open at any one time. This allows the shunting of blood from one region to another. • Veins (and venules) carry blood back to the heart. Blood flows out of the capillaries into the smallest of the veins – venules – which in turn re-unite to form larger veins. The walls of veins are thinner than arteries and often have valves to prevent backflow of blood. BIOLOGY

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EXERCISE AND THE CARDIOVASCULAR SYSTEM (CVS)

Figure 1: Blood vessels. A: oxygenated blood leaves the heart from the left ventricle via the aorta, moves through arteries to arterioles to capilleries to venules and returns to the right atrium by way of veins; B: arteries have well developed walls with a thick middle layer of elastic tissue and smooth muscle; C: capillary walls are one cell thick; D: veins have thinner walls than arteries (with less elastic tissue and smooth muscle), and have valves that prevent the backflow of blood. The heart This muscular, fist-sized organ, which lies between the lungs behind the sternum (breastbone), is a double pump consisting of four chambers – two upper, thin-walled atria and two lower, thick-walled ventricles. The left ventricular wall is thicker than that of the right ventricle as it has to pump blood all round the body, while the right ventricle only pumps blood to the lungs. The cardiovascular system consists of two distinct circuits: • The pulmonary circuit carries deoxygenated blood from the right ventricle to the lungs via the pulmonary arteries and returns oxygenated blood to the left atrium of the heart via the pulmonary veins. (Note that the pulmonary arteries are the only arteries that carry deoxygenated blood.) 2

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EXERCISE AND THE CARDIOVASCULAR SYSTEM (CVS)

• The systemic circuit carries oxygenated blood to the rest of the body, starting from the left ventricle, which pumps blood into the aorta. The aorta branches into many arteries, which in turn transport blood to other organs and major body regions. The deoxygenated blood is returned by the veins to the right atrium. Figure 2 illustrates the path taken by the blood through the circulatory system.

Figure 2: The path taken by blood through the circulatory system.

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The heart has valves that direct blood flow through the heart and prevent backflow of blood. Those lying between the atria and the ventricles are known as atrioventricular (AV) valves. The semi-lunar (half-moon) valves lie between the left ventricle and the aorta and the right ventricle and the pulmonary artery. The heart sounds heard through a stethoscope (‘lub-dub’) are actually the sounds of the heart valves closing. A ‘heart murmur’ can often be heard through a stethoscope as a ‘sloshing’ sound and may be caused by a faulty heart valve not closing properly. The cardiac cycle Each heartbeat is called a cardiac cycle and consists of the following sequence of events: • both atria contract simultaneously; • both ventricles contract simultaneously; • all chambers relax. There are two phases in the cardiac cycle: • systole – contraction of the heart (atrial contraction followed by ventricular contraction); • diastole – relaxation of the heart. At rest, the heart contracts or beats about 72 times a minute (normal range 60–90) and each cardiac cycle lasts about 0.8 seconds (0.3 seconds for systole; 0.5 seconds for diastole). Figure 3 shows a diagrammatic representation of the sequence of events during one cardiac cycle.

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Figure 3: The cardiac cycle. The sequence of events during a single heart beat. The whole cycle takes about 0.8 seconds at a heart rate of 72 beats per minute. The surge of blood entering the arteries during systole stretches their elastic walls, which then recoil during diastole, thus maintaining blood flow when the heart is relaxed. This alternating expansion and recoil of the arteries can be felt as a pulse at several arteries in the body, e.g. the radial artery at the wrist; the carotid artery at the side of the trachea (windpipe). Cardiac output Cardiac output (CO) is the volume of blood pumped by each ventricle per minute and is the function of two factors – heart rate (HR) (beats/ min) and stroke volume (SV) which is the volume of blood ejected by each ventricle during each contraction. CO = HR × SV At rest: HR = 72 beats/min; SV = 70 ml i.e. CO = 72 × 70 = 5040ml/min = 5 litres/min

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Cardiac output varies between individuals and depends on their physical fitness and level of activity. For example, the heart of a highly trained athlete can pump 30–35 l/min while most non-athletes can only achieve a maximum cardiac output of about 20 l/min. Table 1 below shows some typical values for cardiac output at varying levels of activity. Activity level

Heart rate (HR) (beats/min)

Stroke volume Cardiac output (SV) (l/min) (ml) (HR × SV)

Rest

72

70

5

Mild

100

110

11

Moderate

120

112

13.4

Heavy (highly trained athletes)

200

150

30

As the work load increases, HR increases to a maximal value of about 180–200 beats/min (220 minus age in years) while SV increases proportionately less (70–150 ml). The increase in cardiac output with exercise is achieved principally by increasing the heart rate. Blood pressure (BP) The force exerted by the blood against the walls of the blood vessels is known as the blood pressure. It is highest in the large elastic arteries, gradually dropping as it travels round the circulatory system and is almost zero by the time it returns to the right atrium. (Low BP in the capillaries allows the efficient exchange of substances between the blood and the tissues.) This is illustrated in Figure 4.

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Figure 4: Changes in blood pressure through the circulatory system. Arterial BP is highest during ventricular contraction (systolic BP) and lowest during relaxation of the ventricles (diastolic BP). Both systolic and diastolic BP can be measured by an inflatable instrument called a sphygmomanometer which is wrapped around the upper arm (see Figure 5). A stethoscope is placed over the brachial artery just below the cuff and the cuff is inflated until the pressure stops the flow of blood through the artery. The air in the cuff is then gradually released. When the pressure in the artery exceeds the pressure in the cuff the blood starts spurting through the artery again and can be heard through the stethoscope and felt by the subject as a pulse. The pressure at which this occurs is the systolic BP. As more air is released from the cuff, the sounds get louder as blood flow becomes more turbulent, and then become muffled and finally disappear. The pressure at which this happens is the diastolic BP and is the point when blood is flowing continuously through the artery.

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Figure 5: Measuring blood pressure at the brachial artery using a sphygmomanometer. The pressure is measured in millimetres of mercury (mm Hg) and a typical reading for a young healthy adult is about 120/70 mm Hg (SBP/ DBP) although readings vary considerably within the normal range from one person to the next and fluctuate throughout the day. As a person ages, BP tends to rise due to atherosclerosis and so a reasonably healthy 65-year-old may have a resting BP of 140/90 (referred to as 140 over 90). Hypertension or high blood pressure is prolonged elevation in BP often due to ‘hardening of the arteries’ caused by the deposition of calcium and fatty substances in the arterial linings. Other causes include kidney disease; high salt intake; obesity, and genetic predisposition. Systolic BP may increase to 300 mm Hg and diastolic BP may exceed 120 mm Hg. Although hypertension can be symptomless in the early stages, it ultimately puts an excessive strain on the heart and, if untreated, will eventually lead to heart failure and death.

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1.2 Pathology of cardiovascular disease (CVD) So far we have been considering the normal functioning of the CVS in healthy individuals, but what can go wrong with the system? Cardiovascular disease (CVD), which refers to diseases of the heart and blood vessels, is the major cause of death in men and women over 50 in the western world. In the UK, 350,000 people die from CVD every year. It includes diseases such as coronary heart disease (CHD) which itself includes angina pectoris, myocardial infarction and sudden death and stroke. The UK, particularly Scotland, has the unenviable distinction of being near the top of the international league for death from CHD. Atherosclerosis and hypertension are the two disease processes that lead to most cases of CVD. Atherosclerosis Atherosclerosis is the accumulation of a material known as atheroma or plaque beneath the inner lining of the arteries. (Atheroma is the ancient Greek word for porridge, and the material is so called because the deposits look like blobs of porridge.) The process starts with the build up of fatty material (mainly cholesterol), but as the disease progresses, fibrous material and calcium also begin to accumulate. This reduces the diameter of the arteries, thereby restricting blood flow to the area served by a particular artery. It also leads to a loss of elasticity in the arterial wall (hardening of the arteries) and an increase in blood pressure (hypertension). See Figure 6.

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Figure 6: Cross-section of an artery that shows how the build-up of plaque narrows the diameter, obstructing and eventually blocking the flow of blood. Contributing factors to the development of atherosclerosis are high blood pressure, carbon monoxide in cigarettes, diabetes mellitus and high blood cholesterol levels. The condition can affect any artery, but the consequences are particularly serious when it affects the coronary arteries, the arteries supplying the heart muscle. Although atherosclerosis develops progressively from early to middle age, symptoms do not tend to arise until the age of 50 or over, that is until the coronary arteries are markedly narrowed or until a clot or thrombus blocks the artery. Thrombosis The plaque provides a roughened surface that allows blood platelets to accumulate. The platelets release clotting factors which may result in the formation of a blood clot or thrombus at the site of plaque formation. If the thrombus grows large enough to obstruct the artery completely, a thrombosis occurs. For example, a coronary thrombosis closes off one of the blood vessels supplying the heart, while a cerebral thrombosis closes off a blood vessel in the brain.

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If the thrombus breaks loose from the site of formation (now known as an embolus), it travels along the blood stream until it reaches an artery too narrow to allow it to get through. If this embolism occurs in a coronary artery, the part of the heart supplied by the artery will be deprived of oxygen and die – a heart attack or myocardial infarction (MI) results. The consequences of an MI depend on the area of the heart muscle affected – if a very tiny branch of the coronary artery is affected, the MI may go unnoticed (silent infarction), whereas blockage of a larger branch will cause severe chest pains and is often fatal. Figure 7 illustrates how the build-up of atheroma eventually leads to an MI in the coronary arteries.

Figure 7: The build-up of atheroma in coronary arteries, that eventually leads to myocardial infarction (a heart attack).

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An embolism occurring in an artery of the brain results in a stroke (cerebrovascular accident – CVA), the severity of which depends on the area of brain tissue destroyed. Angina pectoris Angina pectoris is chest pain brought on by anything that makes the heart work harder, such as exercise, excitement, emotional upset. It arises when the blood flow through the coronary arteries is reduced by atherosclerosis. At rest, the blood flow and therefore oxygen supply to the heart muscle is usually adequate, despite narrowing of the arteries. However, when the heart needs to work harder, during exercise for example, the restricted blood flow may not be able to meet the additional oxygen requirements of the heart muscle. Unlike skeletal muscle, cardiac muscle cannot work anaerobically (without oxygen), and the resulting lack of oxygen causes the ischaemic pain of angina pectoris, which disappears after a short period of rest. Angina symptoms tend to appear only when atherosclerosis is quite advanced, with the diameter of the coronary arteries reduced by about 70%. Hypertension As previously stated, hypertension is defined as a persistently high resting blood pressure, i.e. systolic BP greater than 140 mm Hg; diastolic BP greater than 90 mm Hg. Various grades of severity of hypertension based on DBP can be defined as in Table 2 below.

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Hypertension

Diastolic BP (mm Hg)

Mild

85 – 89

Moderate

90 – 104

Moderately high

105 – 114

Severe

Greater than 115

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EXERCISE AND THE CARDIOVASCULAR SYSTEM (CVS)

It may be caused by constriction of the arteries due to atherosclerosis and/or loss of elasticity of the arterial walls. Hypertension is a major risk factor for many diseases, including coronary heart disease. Contributing factors include diet (high salt, high fat), obesity, smoking, genetic predisposition, stress. Most cases of hypertension can be controlled by alterations to the diet, exercise, and appropriate medication. The role of cholesterol in CVD Cholesterol is a lipid which is a major component of all cell membranes and the precursor for the synthesis of all steroid hormones such as testosterone, oestrogen and progesterone, and bile salts which are essential for the digestion of dietary fats. While some cholesterol is present in the diet (eggs, dairy produce, liver, etc.) most of the cholesterol in the blood is synthesised in the liver. If the diet contains a lot of cholesterol, the liver compensates by making less, and similarly it makes more if the diet does not contain enough cholesterol (less likely). More important than the amount of cholesterol in the diet is the type of fat eaten. When saturated animal fats are broken down in the body, the liver uses some of the breakdown products to produce cholesterol. Saturated fats can increase blood cholesterol by as much as 25%. Individuals with high levels of cholesterol and saturated fats in the blood are more likely to develop CHD than those with lower levels. There are two important types of cholesterol-carrying proteins in the blood known as low-density lipoproteins (LDL) or ‘bad’ cholesterol and high-density lipoproteins (HDL) or ‘good’ cholesterol. LDL carries about 60–70% of total blood cholesterol and its function is to deliver cholesterol from the liver to the body cells for membrane and hormone synthesis. Under abnormal conditions cholesterol is also deposited in the arterial lining. As blood levels of LDL increase, coronary heart disease risk increases. HDL, which carries about 20% of blood cholesterol, is thought to gather or scavenge cholesterol from body cells and transport it back to the liver for elimination or use in the production of bile salts. As blood levels of HDL increase, the risk of CHD decreases.

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The risk of developing CHD may be predicted by measuring the ratio of HDL to LDL in the blood. A high ratio indicates that HDL level is high and LDL level is low which generally is healthy, while a low ratio indicates low HDL levels and high LDL levels which is generally unhealthy. There is some evidence to suggest that levels of HDL can be increased by exercise. Total plasma cholesterol can be measured very quickly (in about three minutes) by a simple fingerprick test, but information about the HDL:LDL ratio requires more complex laboratory analysis.

1.3 Role of exercise in prevention and treatment of CVD Although there has been a fall in age-adjusted CVD mortality in developed countries over the last twenty to thirty years, CHD is still the leading cause of death. Physical inactivity has been identified as an independent risk factor for CHD which may aggravate the classical risk factors of smoking, high blood cholesterol and hypertension. The actual mechanisms by which physical activity affects health are still unclear and are the subject of much research, but findings to date highlight the benefits of physical activity both in the prevention of many diseases and also in the treatment of individuals with known CVD – cardiac rehabilitation exercise programmes are known to be important with respect to the recovery and future prognosis of such patients. Exercise is thought to decrease many of the risk factors for CHD by: • • • • • • •

improving blood lipid profiles (increase HDL; decrease LDL); decreasing resting heart rate; lowering arterial blood pressure; reducing % body fat; decreasing development of atheroma; improving efficiency of the heart; controlling stress.

Before we can understand the possible mechanisms behind the supposed benefits of physical activity with regard to cardiovascular health, we must understand how the healthy cardiovascular system responds to exercise:

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• what happens to heart rate and blood pressure during exercise? • how is blood flow re-distributed to exercising muscles? During exercise, the cardiovascular system must increase its delivery of oxygen and nutrients to the exercising muscles and also remove waste products effectively. This is done by increasing the blood flow to the exercising muscles by: • increasing cardiac output; • redistributing the circulation of blood round the body. Cardiac output is increased by increasing both heart rate (HR) and stroke volume (SV), both of which increase in proportion to the intensity of exercise. For example, in a relatively untrained person, HR may increase from 70–170 beats/minute and SV from 70 ml to 120 ml per beat, giving an increase in CO from 5 litres per minute at rest to about 20 litres per minute. These changes are caused by: • increased output from sympathetic nerves to the heart which increases HR; • increased release of adrenaline into the blood which increases HR and SV; • increase in blood volume returning to the heart which increases the rate of filling of the heart chambers. This causes stretching of the ventricular walls which respond by contracting more forcibly so that more blood is ejected with each contraction, i.e. SV is increased. The more the ventricular walls are stretched, the greater the force of contraction. The athlete’s heart Why do endurance athletes have lower heart rates both at rest and at any given level of exercise? Endurance training can reduce resting heart rates to as low as 30–40 beats per minute. Like skeletal muscle, cardiac muscle is strengthened by training and is capable of more forceful contraction which increases the stroke volume and, as a result, the heart of an endurance athlete has a considerably larger SV at rest and during exercise than an untrained individual of the same age.

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When comparing the CO during maximal exercise in trained and untrained individuals (Table 3), it can be seen that the endurance athlete achieves a larger CO mainly because of a relatively greater increase in SV. Table 3: Comparison of maximal CO in trained and untrained individuals HR (per min)

SV(ml)

CO (l/min)

Untrained

170

120

20

Trained

195

180

35

Regular exercise training also causes a modest increase in the size of the heart. There is an increase in protein synthesis leading to thickening of individual muscle fibres, and an increase in the number of contractile elements within each fibre. It was previously thought that this increase in size was pathological (heart size also increases in heart failure), but it is now known to be a normal response to endurance training. This increase in size is temporary, however, and the heart returns to its pre-training size if intensity of training decreases. Echocardiography has provided a better understanding of the changes in the dimensions of the heart with training. Sound waves are passed through the heart which can measure the size of the cardiac muscle and the volumes of the chambers (Table 4). Table 4: Comparison of left ventricular mass and volume in trained and untrained individuals Left ventricular mass (g) Left ventricular volume (ml) Trained

300

180

Untrained

210

100

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Redistribution of blood flow during exercise During exercise, there is an increased blood flow to the exercising muscles to supply them with oxygen and nutrients, and a decreased blood flow to organs and parts of the body not active during exercise – e.g. the gut and the kidneys. This is achieved by vasodilation (widening) of the arterioles supplying the active muscles and vasoconstriction (narrowing) of arterioles supplying regions such as the gut and kidneys. For example, Figure 8 shows that, at rest, renal blood flow accounts for about 20% of the total CO of 5.8 l (i.e. 1100 ml/min), while during maximal exercise flow to the kidneys may be reduced to 600 ml/min (3% of CO of 17.5 l). At rest, about 20% of CO goes to skeletal muscles, while during strenuous exercise about 70% of CO goes to skeletal muscles. Strenuous exercise (ml/min) Rest (ml/min)

750 750

Brain

750

Heart

250

Muscle

1200

Skin

500

Kidney

1100

Abdominal organs

1400

Other

600

600

Total

5800

600

12,500

1900

400 17,500

Figure 8: The distribution of cardiac output to the systemic circuit at rest and during strenuous exercise.

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Exercise and blood pressure During exercise, there is a slight increase in systolic blood pressure (SBP) but little change in diastolic blood pressure (DBP) due to the combined effects of increased CO (which would tend to increase BP) and a general vasodilation of arterioles to exercising muscles (which would tend to decrease BP). The overall reduction in total peripheral resistance to the flow of blood caused by the latter largely offsets the increase in CO, allowing increased delivery of oxygen and nutrients to the working muscles without causing a substantial increase in BP which could damage blood vessels and other organs.

Blood pressure mmHg

175 150

Systolic

125 Mean

100

Diastolic

75 5

10

15

20

Cardiac output, litres/min

Figure 9: Changes in systolic, diastolic and mean arterial blood pressures with increasing intensity of exercise. Exercise and hypertension Many studies have shown that regular prolonged aerobic exercise is effective in causing moderate decreases in BP both at rest and during exercise. The precise mechanism is unknown, but it may occur due to: • decrease in sympathetic hormones (e.g. adrenaline) with training. This would contribute to a decrease in peripheral resistance to blood flow and subsequent decrease in BP • exercise which may facilitate elimination of sodium by the kidneys resulting in a decreased fluid volume and BP.

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With increasing age, arteries tend to lose their elasticity, which causes a slight increase in BP. However, it is thought that this loss of elasticity may be largely prevented by regular aerobic exercise throughout life. Exercise also has acute effects on BP. After a bout of exercise, for example, resting BP falls below pre-exercise levels. This post-exercise hypotension is thought to have important long-term consequences both in the prevention and treatment of high BP, if exercise is repeated regularly. Principles of exercise testing There are many reasons why it may be necessary to assess the physiological fitness of an individual, whether an athlete in training or a patient recovering from a myocardial infarction or heart surgery. An exercise test can provide baseline data against which later assessments can be measured, for example: • to monitor the effectiveness of a training programme for an athlete; • to monitor recovery from MI. The exact form of the exercise test will depend on the physical condition of the individual and the reasons for conducting the test. Assessment of aerobic (endurance) fitness The aerobic capacity of an individual is largely determined by their ability to use oxygen, and this depends on the efficiency of their cardiovascular and respiratory systems in delivering oxygen to the exercising muscles at the required rate. A measure of the maximum amount of oxygen that a person can utilise ° . The higher the value of is called the maximal oxygen uptake or VO 2max ° the VO2max, the greater the aerobic fitness of the individual. This test, which uses sophisticated laboratory apparatus to measure oxygen consumption and carbon dioxide production, requires the participant to exercise to exhaustion and is therefore only suitable for evaluating the fitness of competitive athletes.

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° Table 5: Typical values for VO 2max

Group (25–35 years)

° VO (ml/kg/min) 2max Men

° VO (ml/kg/min) 2max Women

Elite endurance athletes

70–80

60–70

Highly trained team games players

55–65

48–60

Active young adults

44–52

38–46

Average for young adults

40–45

34–39

The tests are usually carried out on treadmills or bicycle ergometers, and work intensity is gradually increased until there is no further increase in oxygen consumption despite an increased workload (see Figure 10).

Oxygen consumption

Plateau in oxygen consumption

0

Workload

Figure 10: Graph showing oxygen consumption against work intensity, and that illustrates the plateau in consumption despite an increasing workload. ° testing is not suitable for most individuals and As already stated, VO 2max has several limitations – it requires expensive laboratory equipment, highly trained technical personnel, and medical back-up. ° have For these reasons, several less complex indirect measures of VO 2max been developed which require the individual to exercise at much lower

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intensities. These predictive tests are known as sub-maximal tests. They are based on the assumption that there is a direct linear relationship between heart rate, oxygen consumption and intensity of exercise. By measuring heart rate and oxygen consumption at several levels of ° by extrapolating to their work intensity, it is possible to predict VO 2max predicted maximum heart rate calculated from 220 minus age in years. There are however some important possible sources of error in this ° : predicted VO 2max • Heart rate (especially at low levels) can be affected by other factors apart from exercise, such as emotion, previous meal, temperature, anxiety, etc. • Predicted maximum heart rate may not be accurate for a particular individual. Figure 11 shows how a sub-maximal test may be used to monitor changes in aerobic capacity before and after a training programme. Assumed max. HR

200 190 180

Heart rate (beats/min)

170 160

Before training

150 140 130 120 110 100

° Predicted Vo 2max

After training

90 80 1.0

2.0

3.0

4.0

5.0

Oxygen uptake (litres/min) ° before and after training by Figure 11: Prediction of VO 2max extrapolating the linear relationship between heart rate and oxygen uptake during graded exercise.

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Exercise stress tests Often, individuals with chronic CHD will exhibit normal electrocardiogram (ECG) traces at rest but abnormal ECGs during exercise. Such individuals undergo stress tests on a treadmill when workload is increased in an incremental fashion whilst their ECG is closely monitored. An example of one of the most commonly used protocols, the Bruce Protocol, is shown in Figure 12. 20 5.0

Grade (%)

18 4.2

16 3.4

14 2.5

12 10

2% every 3 min

↑ Speed as shown

1.7

3

6

9 12 Time (min)

15

18

Figure 12: Illustration of the Bruce Protocol, an example of a stress test used to monitor the heart’s response to increasing levels of exercise. Step tests The simplest and most commonly used sub-maximal test is the step test, which uses steady-state exercise heart rates or recovery heart rates to evaluate the efficiency of the cardiovascular response to exercise. There are many different protocols for step tests but all are based on the same physiological principles. They involve the subject stepping up and down from a step or bench at a fixed pace for several minutes (3–5 minutes). The height of the step and the rate of stepping (often set by a metronome) vary with different protocols. At the end of the exercise, HR is measured for 15–30 seconds at oneminute intervals for about four minutes after cessation of exercise to measure the rate of recovery.

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The fitter the individual, the lower the HR will be immediately after exercise and the faster it will return to its resting level. Figure 13 shows the heart rate response during a stepping exercise and in recovery for three individuals of varying levels of fitness, Subject A being the fittest and Subject C the least fit.

Figure 13: Heart rate response during a step test and in recovery for three individuals of different levels of cardiovascular fitness. It is also possible to measure heart rate continuously during exercise by wearing an HR monitor. An identical test can be repeated at a later stage in order to evaluate any changes in the aerobic fitness, with lower HRs indicating an improvement in fitness. Shuttle tests The 20-metre shuttle run is a commonly used field test of aerobic fitness. However, it is maximal and exhaustive and is therefore only suitable for moderately fit individuals. Participants run between two markers positioned twenty metres apart at a pace determined by a pre-recorded tape. The test starts at a fairly slow pace which increases every minute and the individual runs between the two markers until they cannot keep up with the pace. The level they reach (i.e. number of completed shuttles) is recorded and may be used 째 . to predict VO 2max BIOLOGY

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A variation of this test – the shuttle walking test – is more suitable for less fit individuals. Role of exercise in cardiac rehabilitation Over the last twenty years there has been a major change in the treatment of patients who have had a heart attack or who have undergone cardiac surgery. Before the 1970s, complete bed rest for at least six weeks following a heart attack or surgery was the standard treatment. This was to allow time for the damaged heart muscle to form scar tissue. Now, however, some form of supervised aerobic exercise sessions are included in all cardiac rehabilitation programmes, which also offer advice on diet, smoking, alcohol, stress and relaxation. The exercise programmes are not designed to produce elite athletes, but aim to allow patients to improve their physical fitness to a level at which they can cope with the physical demands of everyday life. The initial stages of the exercise programme are likely to start within a week of the heart attack or surgery and will include gentle walking. Slightly more vigorous activity can start four to six weeks later.

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SECTION 2

2.1 Energy The need for energy Energy is needed for: • the basal requirements which keep the body alive – i.e. energy for keeping the heart beating, for breathing, for maintaining body temperature and all the other vital processes. This is known as the Basal Metabolic Rate (BMR); • active movement – i.e. muscle contraction; • synthesis of enzymes and other cellular materials, to allow growth and repair of body tissues; • pregnancy and lactation. Energy comes from the food we eat. The stored chemical energy in carbohydrates, fats, and proteins is released by the series of biochemical reactions in cellular respiration to produce Adenosine Triphosphate (ATP) which in turn provides the energy for all the above energy needs. Energy balance When the energy obtained from food is equal to the total energy expended by the body, the individual is in energy balance. When the diet provides more energy than the body is using, the excess energy is stored as body fat and the individual gains weight – a positive energy balance. Conversely, when the diet provides less energy than the body is using, fat stores are mobilised to make up the deficit and the individual will lose weight – a negative energy balance. Figure 14 illustrates the principle of energy balance.

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Figure 14: The principle of energy balance. Energy measurement The SI unit for measurement of energy is the kilojoule (kJ). Traditionally, energy has been measured in calories or kilocalories (1000 calories = 1 kcal) and this term is still widely used both by nutritionists and the general public particularly with reference to food labelling and weight-reducing diets. For this reason, it is important to be familiar with both terms. 1 kcal = 4.18 kJ 26

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Energy is provided mainly by three nutrients found in food – carbohydrate, fat and protein. Alcohol (which is not a nutrient) also provides energy. Carbohydrate: Fat: Protein: Alcohol:

16 37 17 29

kJ kJ kJ kJ

per per per per

gram gram gram gram

The amount of energy provided by the diet depends on the proportions of carbohydrate, fat, protein and alcohol that are present – e.g., a highfat diet will provide more energy than a low-fat diet. To find out how much energy a particular food provides, the food is burnt in a bomb calorimeter (Figure 15). This breaks the chemical bonds holding the atoms together resulting in the release of heat energy which can be measured.

Figure 15: The bomb calorimeter. Published tables and computerised dietary analysis programmes have been designed to calculate an individual’s total energy intake. The amount of energy required by an individual depends on three main factors: • basal metabolic rate, • level of physical activity, • body weight and composition.

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Assuming an individual is in energy balance (i.e. body weight is constant over a period of time), energy requirements can be gauged accurately either by measuring the total amount of energy consumed or measuring the total energy expenditure of the individual over several days. Both techniques can be time-consuming and costly and require highly motivated subjects. However, the average energy requirements can be estimated from published tables. In the UK, the Department of Health published Estimated Average Requirements (EAR) per day for energy for various age/sex groups within the population. For example: Table 6 Age (years)

Estimated Average Requirement (males)

Estimated Average Requirement (females)

11–14

9.27 MJ /day

7.72 MJ/day

15–18

11.51 MJ /day

8.83 MJ/day

19–50

10.60 MJ /day

8.10 MJ/day

1 MJ = 1000 kJ These energy requirements assume a fairly inactive lifestyle, which is true for the majority of individuals in the UK. These estimated energy requirements are useful for studies of large groups of people but should only be used as a guide when considering an individual, whose energy requirements may be considerably more or less than the estimated value. Dietary recommendations for health A small positive energy balance over a long period of time will lead to being overweight and eventually to obesity, which is an important risk factor in the development of coronary heart disease, high blood pressure, stroke and Type 2 diabetes mellitus. There has been a marked increase in the prevalence of obesity in the UK in the past fifty years and particularly in the last ten to twenty years.

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There are many possible reasons for this, the most likely being: • a marked reduction in the level of physical activity both at work and during leisure time (e.g. increased use of cars; increased time spent watching television and playing computer games); • the percentage contribution from energy-dense fat in the diet is relatively high (about 38%) despite an overall decrease in the average total energy intake. Figure 16 shows the percentage contribution of protein, fat and carbohydrate to the average British diet in 1995, while Figure 17 illustrates the changing proportions of these nutrients to total energy intake since 1943. Average energy intake per person per day = 7800 kilojoules 1kcal = 4.18kJ

Protein 15% Total fat 38% Total carbohydrate 47%

Figure 16: The contribution of protein, fat and carbohydrate to total energy intake in 1995. (Source: MAFF National Food Survey 1995, HMSO, 1996).

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1943*

1952

Year

1962

1972

1982

1992 0

20

*Records begin

Fat

40

60

80

Percentage of energy

Carbohydrate

Protein

Figure 17: Changes in energy intake from protein, fat and carbohydrate, 1943-1992. (Source: MAFF Household Food Consumption and Expenditure 1990, HMSO, 1991 and MAFF National Food Survey 1992, HMSO, 1993). In order to reduce the high prevalence of obesity, heart disease, etc. in the UK, the recommendations are to reduce the contribution from fat from 38% to 35% and eventually to 30%, while increasing the contribution from complex carbohydrates (i.e. cereals, starches, etc.) from 47% to about 50% of total energy consumed.

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Energy expenditure and its measurement The total amount of energy expended by the body is the sum of three components: 1. 2. 3.

Basal metabolic rate, Thermic effect of food, Physical activity.

1.

Basal metabolic rate (BMR)

This is the energy expended in the resting, fasting state and is the energy required to carry out normal body functions such as breathing, circulation of blood, etc. It is the energy that would be used by a person simply lying in bed all day. It is the largest component of an average individual’s energy expenditure and in sedentary adults accounts for about 60–70% of total energy output. The main factors affecting BMR in an individual are: (a)

Body size and composition

BMR increases as body weight increases – the more tissue present, the more energy is expended. However, even at a given body weight, BMR can differ greatly between individuals due to differences in their body composition – i.e the relative proportion of lean to fat tissue. Lean tissue (e.g. muscle) is more metabolically active than fat (adipose) tissue, therefore the greater the proportion of lean tissue an individual has, the higher their BMR. For example, if two individuals of the same weight, height, age and sex are compared, the one with the greater amount of lean tissue is likely to have the higher BMR. (b)

Age

BMR per kg body weight is higher in children owing to the energy cost of growth, but from 18–20 years, BMR per kg decreases at the rate of about 2% per decade. This age-related fall is partly due to changing body composition as we get older – the tendency to put on extra fat with the loss of lean tissue, usually as a result of becoming less physically active.

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(c)

Sex

BMR per kg tends to be higher in males because they have a higher proportion of lean tissue. For example, the average % of body fat for a 20-year-old 60-kg male is about 12–15%, and he is likely to have a higher BMR than a 20-year-old 60-kg female, who is likely to have average body fat of 25–30%. (d)

Nutritional status

BMR is reduced by fasting or by being on a very low-energy intake for any length of time. This fall is caused by the loss of metabolically active lean tissue (i.e. muscle) in addition to the fat loss that accompanies negative energy balance. It is also the body’s adaptive survival mechanism when food is scarce. Energy output is reduced to conserve energy and survive longer. This fall in BMR in response to reduced food intake is one of the reasons for the failure of many weight-reduction diets. The body adapts to the lower food intake, so in order to keep losing weight, food intake must be reduced even further, and it becomes a vicious circle. Measurement of BMR BMR must be measured under highly standardised conditions – e.g. 12–18 hours after eating; at complete physical and mental rest; in a comfortable environment (not too hot or too cold); free from anxiety; etc. Alternatively, there are a number of age-, weight- and sex-adjusted equations for the prediction of BMR when an actual measurement is not possible. Examples of some of these equations are shown below:

Males 10–17 years: BMR (MJ/d) = 0.074 × body weight (kg) + 2.754 18–29 years: BMR (MJ/d) = 0.063 × body weight (kg) + 2.896

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Females 10–17 years: BMR (MJ/d) = 0.056 × body weight (kg) + 2.898 18–29 years: BMR (MJ/d) = 0.062 × body weight (kg) + 2.036

2.

Thermic effect of food

The body uses up energy to digest, absorb, metabolise and store ingested nutrients. Depending on the quantity and composition of the food eaten, energy expenditure may increase as much as 30% above basal in the two to three hours following a meal. Over a twenty-fourhour period, the thermic effect of food accounts for about 10% of the total energy expended. The thermic response to a meal can vary considerably depending on the quantity and type of food eaten. For example, the thermic response can vary from a 17% increase in energy expenditure for a high-protein meal, to a 9% increase for a high-carbohydrate meal, to only a 3% increase for a high-fat meal. This means that people on a high-fat diet will not use up so much energy to digest and absorb their food as someone on a healthier highcarbohydrate diet. This highlights one of the many dangers of high-fat diets. 3.

Physical activity

This is the energy expended above resting to move about and perform tasks such as sitting, standing, walking, running, lifting, etc. It is the most variable of the components of energy expenditure, accounting for about 30% of total energy output in sedentary individuals, up to more than 50% in those engaged in heavy manual work or vigorous training programmes. Table 7 shows some typical values of the energy cost of various activities.

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Table 7 Activity

Body wt = 55 kg kJ/ min

Body wt = 80 kg kJ/ min

Sitting

4.6

6.3

Cycling

25.5

36

Walking (3.5 mph)

18.4

26.8

Running (6 mph)

38.5

54.3

Aerobics (vigorous)

32.6

45.6

Cross-country ski-ing

54.3

76

Note that a heavier person usually uses up more energy to perform an activity due to the extra effort required to move the heavier body. The energy cost of an activity is often expressed as a multiple of BMR, known as a Physical Activity Ratio or PAR. For example, lying at rest (assumed to be equivalent to BMR) has a PAR of 1.0. PARs of some other activities are shown in Table 8: Table 8 Activity

PAR

Sitting quietly (watching television, reading)

1.2

Sitting active (driving )

1.6

Standing activities (ironing, washing up, etc.)

1.4

Moving about activities (cleaning, etc.)

2.1

Walking (average speed)

2.8

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Physical activity is the biggest single component of the total energy expenditure which can be changed voluntarily, and is likely to be the main reason for individual differences in energy requirements. The energy expended in physical activity is largely determined by occupation and leisure activities. The energy required for physical activity of any kind depends on several variables, such as the intensity and the duration of the activity and the muscle masses involved. When considering the influence of physical activity on energy expenditure, it is important to distinguish between short bursts of strenuous activity and moderate activity of relatively long duration. For example, a thirty-minute game of squash at 42 kJ/min would use 1260 kJ whereas a three-hour round of golf at 16.7 kJ/min would use 3010 kJ. Energy expenditure (EE) does not return to baseline values immediately after the activity stops. The size of this post-exercise elevation of EE depends on the intensity of the exercise. If exercise is severe, EE remains elevated above resting levels for some time after the activity has stopped. This metabolic response is known as excess post-exercise oxygen consumption (EPOC) and is due to the need for oxygen to replenish glycogen stores in the liver and muscles. However, the intensity and duration of exercise undertaken by most ‘non-athletes’ results in a return to resting levels of EE within five to forty minutes of cessation of exercise, and accounts for only about 20–100 additional kJ expended. Although this is a small amount in terms of total energy expended, it has the potential to help maintain energy balance if exercise is undertaken on a regular basis. Several studies have suggested that exercise may increase BMR – and as this increase is lost after several days of inactivity, regular exercise patterns are important.

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Measurement of energy expenditure (EE) There are several methods of measuring EE. The most commonly used ones are: 1.

Direct calorimetry

All of the energy produced by the body’s metabolic reactions ultimately result in heat production. Therefore measurement of the heat produced by the body gives a measure of energy released. Under laboratory conditions, heat production can be measured in a specially designed, airtight chamber called a direct calorimeter, in which a person can live for several days (see Figure 18).

Figure 18: The direct calorimeter. Heat production is measured by temperature changes in water flowing through a series of pipes at the top of the chamber. As the chamber is heavily insulated, any change in water temperature must be due to heat produced and radiated by the individual. Oxygen is circulated through the chamber, and exhaled air is passed through chemicals which remove water vapour and carbon dioxide. This very accurate technique has been used extensively over many years for research purposes, but is unfortunately very expensive and technically difficult to operate, making it unsuitable for large-scale studies of free-living individuals. 36

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2.

Indirect calorimetry

Since 95% of energy production in the body depends on the presence of oxygen, it follows that the measurement of the oxygen consumed by the body over a period of time gives an indirect measure of energy expenditure. This is known as indirect calorimetry. Compared to direct calorimetry, this technique is much simpler and less costly but is also highly accurate if carried out carefully. The subject breathes in air which has a known and constant composition of 20.93% oxygen, 0.03% carbon dioxide and 79.04% nitrogen. The air breathed out by the subject will have less oxygen (usually 16–18%) and more carbon dioxide (3–5%). Measurement of oxygen consumption by the body requires knowledge of two factors: • the volume of air breathed out over a specified time • the composition of the expired air. For resting activities, the volume of expired air is usually collected for ten to fifteen minutes in a large plastic bag. A small sample of the expired air is analysed for its oxygen and carbon dioxide content, and the total volume of air expired is measured by a gas meter. The following example illustrates how oxygen consumption can be calculated. (For ease of calculation, it is assumed that % oxygen in inspired air is 21%.)

Example Volume of air expired in 10 minutes = 100 litres % O2 in inspired air = 21% % O2 in expired air = 18% Volume Volume Volume Volume

of of of of

O2 O2 O2 O2

in inspired air in expired air used in 10 min used per min

= = = =

21% of 100 l = 18 % of 100 l = (21–18) l = 3/10 l =

21 l 18 l 3l 0.3 l

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It is known that approximately 20 kJ of energy is released when 1 litre of oxygen is consumed, so in the above example, EE would be: EE = 20 Ă— 0.3 = 6 kJ/min The bag method is unsuitable for measuring the EE during physical activity. Portable respirometers allow energy expenditure during numerous occupational and sporting activities to be measured. A respirometer measures the total volume of expired air passing through it and collects a small gas sample for subsequent analysis of oxygen and carbon dioxide. Measurements made using these respirometers form the basis of published tables of the energy cost values of many activities. Figures 19 and 20 illustrate the measurement of various activities using these portable respirometers.

Figure 19: Measuring energy expenditure during different activities using a portable respirometer.

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Figure 20: Measuring energy expenditure using a modern, lightweight portable respirometer. In order to calculate the total energy expenditure of an individual, it is necessary to have an accurately timed record of all the activities of the day in addition to the energy cost of each activity. An activity diary, covering all 1,440 minutes of the day, should ideally be kept for four to seven days in order to represent a typical pattern of normal life for the individual. The energy cost of each activity can either be measured by indirect calorimetry, as previously described, or estimated from published values. Figure 21 shows a page from a typical activity diary, and Table 9 shows how total energy expenditure can be calculated for an individual.

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a.m.

0

9.00

S

1

2

3

4

5

6

7

8

9

STA

9.10 9.20

Each page must add up to 120 min

WS

9.30

S STA WS WF

S

9.40 9.50 STA

10.00

= = = =

10.10 10.20

= 34 = 45 = 23 = 18 120 min

N.B. Only record when there is a change in activity

10.30 WF

10.40

7 + 27 15 + 30 23 18 Total

10.50 S = Sitting STA = Standing activity

W S = Walking slowly W F = Walking fast

Figure 21: An example of a page from an activity diary. Table 9 Activity

Duration (min)

Energy cost (kJ/min)

Total (kJ)

Sleeping

480

5

2,400

Washing, dressing, etc.

80

9

720

Sitting activities (TV, etc.)

630

7

4,410

Standing activities (cooking, ironing, etc.)

150

8

1,200

Moving around (walking/standing)

60

16

960

Walking

40

17

680

TOTAL

1,440

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Heart rate recording Indirect assessment of EE may be attempted by the use of heart rate (HR) recorders. In any individual there is a relationship between heart rate and oxygen consumption during any activity above resting – the greater the oxygen consumption, the higher the heart rate. This relationship between HR and EE will vary according to the fitness of the individual and will depend on the type of activity being undertaken. Figure 22 shows a plot of HR against oxygen consumption for two individuals of differing physical fitness. Subject A is able to work at a particular intensity at a lower HR than the less fit Subject B.

Figure 22: The linear relationship between heart rate and oxygen consumption in two individuals. If the relationship between HR and EE is known for an individual, it is possible to record HR over a 24-hour period using a ‘Sports Tester’. This is a lightweight transmitter applied to the chest by a belt with electrodes on the inner surface. A watch-like device attached to the wrist records HR continuously for up to 24 hours (or longer). The data can then be downloaded to a computer for analysis to estimate energy expenditure from the recorded heart rates.

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2.2 Body composition and weight control Body composition is possibly the best indicator of the cumulative effects of physical activity and nutrition. Low levels of aerobic activity and energy-dense diets are likely to be the main reasons for the escalating prevalence of obesity (excess body fat) in the developed world. Body weight itself does not distinguish between excess weight (which is undesirable fat) and desirable muscle. In fact most successful weight management programmes result from losing fat while maintaining or even gaining lean tissue (muscle). This may often result in little change or even an increase in body weight. The most commonly used index of over- or underweight is called the Body Mass Index (BMI), calculated by dividing body weight (kg) by height squared (m2). Table 10 shows the currently accepted classification of overweight using BMI, and the associated health risks. Table 10 Classification

BMI (kg/m2)

Associated health risks

Underweight

Less than 18.5

Low

Normal

18.5 – 24.9

Average

Overweight

Greater than 25.0

Moderate Obese class I Obese class II Obese class III

25.0 – 29.9 30.0 – 34.9 35.0 – 39.9 Greater than 40

Increased Moderately increased Severely increased Very severely increased

Classification by BMI may result in an individual being classified as overweight or obese, when in fact they have a relatively low % body fat but a large muscle bulk. Examples of such individuals are body-builders, weight-lifters and other athletes with a well-developed musculature. For example, a bodybuilder weighing 130 kg and 1.90 m tall would have a BMI of 36 kg/m2 (130/ 1.902) and would be wrongly classified as obese class II.

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Similarly, two individuals of the same weight and height may have BMIs in the ‘average’ range, but may have quite different % body fat. In summary then, the many reasons for assessing body composition include: 1.

To assess the health risk associated with having too much or too little body fat.

2.

To monitor weight loss in an obese individual.

3.

To monitor changes in body composition associated with certain diseases (e.g. some cancers).

4.

To monitor the effectiveness of exercise training programmes in athletes.

Measurement of body composition For most purposes, the evaluation of body composition assumes that the body consists of two main compartments: • The Fat Mass (FM) – all the chemical fat in the body • The Fat-Free Mass (FFM) – muscle, bone and water (i.e. everything apart from FM). There are many methods of assessing body composition, and they vary in complexity and accuracy. There are a number of highly accurate laboratory methods which are costly, time-consuming and are therefore restricted to relatively small numbers in a research setting. Densitometry For over thirty years, the most accurate method of assessing body composition has been the measurement of body density by underwater weighing. This assumes that the fat mass and fat-free mass have fixed and constant densities of 0.9 g cm–3 and 1.1 g cm–3 respectively, therefore measurement of an individual’s body density can predict the relative proportions of lean and fat tissue in the body. Lean tissue (muscle) weighs more under water than fat tissue (see Figure 23).

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Figure 23: Why does one person sink and another float?

Density is calculated from body mass (kg) measured in air divided by body volume (l) which can be measured by weighing the individual immersed in a tank of water. The difference between the weight in air and the underwater weight is equal to the body volume (Archimedes’ Principle). Figure 24 shows this technique being performed. Figure 24: Measuring body density by underwater weighing.

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Having calculated body density, % body fat is computed using a mathematical formula: % Fat = 495/density (g cm–3) – 450 The following example illustrates this calculation: A 60 kg person weighs 2 kg when weighed underwater. According to Achimedes’ Principle, the weight loss in water of 58 kg is equal to the weight of water displaced. 58 kg of water = 58 litres, or 58,000 cm3 The density of this person calculated as weight/volume is therefore: Density (g cm–3) = 60,000 g (60 kg)/58,000 cm 3 = 1.0345 g cm–3 When this value is incorporated into the formula above, % body fat is: % Fat = 495/1.0345 – 450 = 28.5 % The disadvantage of this method is that being submerged under water may be difficult and produce anxiety in some individuals (e.g. children, the elderly). A new method of measuring body density has been developed which may eventually replace underwater weighing. Instead of using water to measure body volume, the ‘Bod Pod’ uses air displacement. For this procedure, the subject sits inside a small chamber (the ‘bod pod’), and body volume is computed by measuring the initial volume of the empty chamber minus the volume with the person inside (see Figure 25).

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Figure 25: The ‘bod pod’ that measures body density through air displacement.

The advantages of this method over underwater weighing are: • short measurement time (5–8 minutes) • ease of operation • does not require submersion in water • suitable for special groups such as children, the elderly, the obese, and the disabled. The major disadvantage of this method is its very high cost. From the rather complex densitometry method, a number of simpler ‘bed-side’ methods have been developed to predict body fat. Skinfold thicknesses This is the most widely used method for estimating body composition and involves measuring the layer of fat under the skin (subcutaneous layer) at specific sites with a skinfold caliper (see Figure 26).

Figure 26: Measuring skinfold thicknesses with calipers. 46

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Four sites are commonly used as shown in Figure 27:

Figure 27: The sites commonly used for measuring skinfold thicknesses (1 biceps; 2 triceps; 3 subscapular; 4 supra-iliac). 1. 2. 3. 4.

over the biceps muscle at the front of the arm over the triceps muscle at the back of the arm under the shoulder blade at the back (subscapular) above the hip bone at the side of the body (supra-iliac).

The sum of the four skinfolds is then used in a mathematical formula to predict body density and in turn % body fat. The advantages of this method are that it is: • • • • •

non-invasive relatively cheap portable quick accurate once skill has been mastered.

Disadvantages: • errors associated with measurer skill • does not take into account unusual fat distribution • difficult in the very obese and the very lean.

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Bioelectrical impedance analysis (BIA) This method has become increasingly popular over the last few years, particularly in health and fitness clubs, owing to its ease of use. BIA is based on the principle that the fat-free mass (which is about 73% salty water) offers very little resistance (impedance) to the flow of a small electric current whereas the fat mass (which is an insulator) conducts very little of the current – i.e. it has a higher resistance (impedance) to the flow of current. Therefore, measuring the impedance of the body to the flow of the applied electric current can give an estimate of the lean / fat ratio in the body – the higher the impedance value, the higher the % body fat. Figure 28 shows the positioning of the individual for measurement using BIA.

Figure 28: The position of body and electrode placement using bioelectrical analysis to estimate body fat. Subject must be lying down.

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Advantages of BIA: • • • •

requires little or no technical skill by the operator takes less than a minute to perform unit is easily transportable only requires removal of a sock (unlike skinfolds).

Disadvantages: • any disturbance in hydration level in the body (i.e. dehydration or oedema) will affect the accuracy of the result • tends to over-estimate body fat in very lean, muscular people and under-estimate % fat in obese people. Waist/hip ratio It is now known that the distribution of fat in the body rather than the total quantity of fat is more important with regard to overall health risk. People can be classified as ‘apples’ (android) or ‘pears’ (gynoid) according to their fat distribution (see Figure 29). ‘Apples’ (people with extra abdominal fat) carry a higher risk of CHD, Type 2 diabetes, etc. than ‘pears’ (people with extra fat around the hips and thighs).

Figure 29: The ‘apple’ and ‘pear’ patterns of fat distribution.

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A simple way of estimating the fat distribution of individuals is to measure the ratio of waist circumference to hip circumference. Those with ‘apple’ shape will have a higher ratio than those with a ‘pear’ shape. ‘At-risk’ values are a waist/hip ratio of greater than 1.0 for men and 0.8 for women. Weight control and obesity A definition of obesity is ‘A chronic disease characterised by excessively high body fat in relation to lean body tissue’. Scale of the problem The prevalence of obesity in England, as defined by a body mass index (BMI) of greater than 30 kg/m2, increased from 6% of men and 8% of women in 1980 to 17% of men and 20% of women in 1997. If this trend continues, it is predicted that the prevalence of obesity in the year 2010 will be about 19% of men and 25% of women (see Figure 30). % BMI >30 30 25 20 ○

15 ○

10 5 0 1980

1985

1990

1995

2000

2005

2010

Year Men

Women

Figure 30: The increasing rate of obesity since 1980. The prevalence of obesity in Scotland is similar to that in England, with 14% of men and 17% of women classified as obese (BMI > 30). Even more worryingly, about 20% of Scottish children are overweight.

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Health risks of obesity There are many health problems associated with obesity, including an increased risk of: • • • • •

coronary heart disease type 2 (non-insulin dependent) diabetes (80% of sufferers are obese) some cancers (colon; breast; possibly uterine and ovarian) bone and joint disorders (excess pressure on knee, ankle and hip joints) respiratory problems (excess weight over lungs).

Causes of obesity The causes of obesity are complex and are often interrelated. Environmental, genetic, psychological, metabolic and dietary factors may all be involved. However, the two most likely causes of the steep rise in the prevalence of obesity in the last twenty years are: • the decrease in physical activity both at work and at leisure • the energy-dense (high-fat) diet currently consumed. Although the average total energy intake has actually decreased over this time period, the energy output has decreased to a greater extent, resulting in a positive energy balance, which ultimately results in obesity. Treatment of obesity Obesity is treated by reducing energy intake, increasing energy expenditure or a combination of both. Current evidence would suggest that weight loss is more likely to be maintained if levels of physical activity are increased by permanent lifestyle changes in addition to reducing the amount of fat in the diet. Effect of exercise on body composition and weight control Individuals who maintain a physically active lifestyle tend to maintain a desirable level of body composition (12–15% fat in males, 20–30% in females). For individuals who are trying to lose weight by only reducing their food intake, the addition of exercise has many benefits: • increased energy deficit • increased relative loss of fat while preserving ‘active’ lean tissue

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• prevents fall in BMR which often accompanies low-energy intakes • provides significant benefits to overall health. Physical activity does not need to be strenuous to achieve these benefits. A negative energy balance of 29.4 MJ (7000 kcal) is required to lose 1kg of body fat, regardless of whether this deficit occurs slowly or rapidly. For example, a deficit of 420 kJ /day between energy intake and energy expenditure will result in the loss of 1kg after ten weeks (420 × 7 × 10 = 29,400 kJ), while a deficit of 2100 kJ/day should result in the same fat loss after only fourteen days (2,100 × 14 = 29,400 kJ). The effectiveness of exercise in weight-control programmes will depend on the target amount of body fat to be lost. Example: Let us assume that an individual wants to lose 10kg of body fat – this represents a total energy deficit of approximately 294 MJ. If the desired energy deficit is 2 MJ/day (which can be achieved by increasing energy output by 1 MJ/day and reducing energy intake by 1 MJ/day), then it would take approximately 147 days (21 weeks) to lose 10kg of fat. The same fat loss could be achieved by creating an energy deficit of only 1 MJ/day, but this would take nearly a year to achieve. Conversely, if the energy deficit was increased to 4 MJ/day, 10kg of body fat should be lost after only ten weeks (294 / 4 = 74 days = approx. ten weeks). Many nutritionists recommend a fat loss of no more than 0.5–1.0kg per week, which is achieved by an energy deficit of approximately 2–4MJ/day. Aerobic forms of exercise of moderate intensity and reasonably long duration – e.g. brisk walking, jogging, swimming, cycling, golf, dancing – seem to be the most effective for fat loss in addition to conferring many other health benefits. Many health authorities, including the Health Education Board for Scotland (HEBS), now recommend the accumulation of at least thirty minutes of moderate-intensity physical activity over most days of the week.

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2.3 Diabetes mellitus This section examines the role of exercise in the treatment and prevention of diabetes mellitus, a disorder occurring in adults and children which results in a failure to control blood glucose levels and an impaired ability to store glucose in the form of liver and muscle glycogen. Diabetics have additional health complications such as an increased risk of developing atherosclerosis, hypertension, stroke, kidney disease, nerve damage and impaired vision due to cataracts and damaged retinas. There are therefore implications for the quality of life and longevity. Firstly, we need to understand the normal control of blood glucose and then consider the pathophysiology of the disorder. Control of blood glucose levels Blood glucose levels must be kept between fairly narrow limits, and this is normally achieved by storing excess glucose after a meal in the form of glycogen in the liver and skeletal muscles. This prevents blood glucose levels from becoming too high (hyperglycaemia). The brain requires a constant supply of glucose, so between meals and after an overnight fast, blood glucose levels are maintained by the liver releasing glucose back into the bloodstream, thereby preventing blood glucose from falling too low (hypoglycaemia). Blood glucose levels are controlled mainly by the hormones insulin and glucagon, which are secreted by small clusters of cells scattered throughout the pancreas and known as the Islets of Langerhans. Beta (β) cells secrete insulin and Alpha (ι) cells secrete glucagon. The control of blood glucose levels by the opposing actions of insulin and glucagon is illustrated in Figure 31.

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Figure 31: The control of blood glucose levels through the actions of insulin and glucagon. The secretion of insulin and glucagon is directly controlled by the level of blood glucose that passes through the pancreas. An increase in blood glucose (e.g. after a meal) stimulates insulin secretion and decreases glucagon secretion. A reduction in blood glucose (between meals) leads to a decreased insulin secretion and increased glucagon secretion. This homeostatic control mechanism is an example of negative feedback control – increased blood glucose stimulates insulin secretion; insulin then induces glucose entry into cells, which lowers the blood glucose and reduces the stimulus to the pancreas for insulin secretion. Insulin affects a number of different cell types, the principal targets being skeletal muscle cells, liver cells and fat cells.

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Skeletal muscle cells and fat cells have a very low permeability to glucose in the absence of insulin. Insulin acts by stimulating the uptake of glucose into muscle and fat cells. By contrast, the cell membrane of liver cells is quite permeable to glucose, so glucose enters whether or not insulin is present. However, insulin still increases the uptake of glucose by liver cells and increases glycogen formation. Insulin is a protein hormone which binds to specific receptors in the cell membrane of its target cells. These insulin receptor complexes result in a series of reactions allowing glucose to pass through the cell membrane. This is illustrated in Figure 32.

Figure 32: The action of insulin. Under certain circumstances, e.g. obesity, the number of insulin receptors decreases, thereby decreasing glucose uptake into the cell. This reduction in the number of receptors leads to insulin resistance.

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There are therefore two basic types of diabetes mellitus. Type 1 is caused by failure of the pancreas to produce adequate amounts of insulin and is known as insulin dependent diabetes mellitus (IDDM). Type 2 is caused by a failure of the tissues to respond to insulin (that is, insulin resistance) and is called non-insulin dependent diabetes mellitus (NIDDM). Type 1 IDDM (insulin dependent) This form of the disorder, which accounts for 5–10% of cases, is rapid in onset and progress and is caused by the destruction of the insulinproducing β cells of the pancreas, which results in inadequate insulin production. This commonly occurs in childhood and was previously referred to as early-onset or juvenile-onset diabetes. The treatment for Type 1 diabetes is regular injections of insulin, given subcutaneously. Insulin cannot be taken orally because it is a protein and would be digested by the gastro-intestinal enzymes. Symptoms normally include fatigue, weight loss and weakness. Weight loss is caused by the body breaking down fat stores (and protein) to supply the cells with energy because they cannot utilise glucose. Type 2 NIDDM (non-insulin dependent) This much more common disorder (90–95% of cases) typically develops later in life (after age 40) and was previously known as adult-onset or maturity-onset diabetes. It affects 3–7% of the adult population, and worldwide accounts for hundreds of thousands of deaths annually due to an increased incidence of cardiovascular disease. It causes disability in millions. It occurs mainly in overweight individuals – more than 80% of Type 2 diabetics are or have been overweight. In this condition, individuals can produce insulin, and have insulin levels in the blood which are normal or higher than normal, but the tissues (especially the liver and skeletal muscles) become less sensitive to it. This is known as insulin resistance. The target cells for insulin appear to have a deficiency of insulin receptors and this reduces the ability of the skeletal muscle cells and fat cells to take up glucose.

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Most individuals develop insulin resistance before they develop the disease, often as a consequence of becoming obese – i.e. they produce insulin, but it cannot be used effectively by the cells. The pancreas tries to compensate for this resistance by producing more insulin. Eventually the β cells become ‘worn-out’ and insulin production decreases. This results in an increase in blood glucose and diabetes develops. In both types of diabetes, the inability to store glucose after a meal and the limited uptake of glucose into the cells results in a rapid rise in blood glucose levels (hyperglycaemia). At very high levels, the kidneys are unable to absorb all the glucose passing through them and the excess glucose appears in the urine. Glycosuria is often the first stage in the diagnosis of the condition, from urine tests carried out as part of a routine examination. The excess glucose excreted in the urine carries with it a large volume of water, which accounts for the large amount of urine produced (polyuria) and the subsequent thirst which follows (polydipsia). Glucose tolerance test This test is used for the diagnosis of either type of diabetes mellitus and is based on the fasting individual’s response to drinking a prescribed amount of glucose (50–100g) dissolved in 1 litre of water. Blood glucose levels are then measured every thirty minutes over a two-hour period. Figure 33 illustrates the results of a glucose tolerance test for a nondiabetic and a diabetic individual.

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18

Blood glucose concentration (mmol/l)

16 14 diabetic

12 10 8 6

non-diabetic 4 2 0

0

30

60 90 time (minutes)

120

150

Glucose ingested

Figure 33: Examples of glucose tolerance results for diabetic and nondiabetic subjects. In the non-diabetic individual, blood glucose reaches a peak of 7mmol l –1 thirty minutes after ingestion of glucose load, and falls to 4mmol l –1 after two hours. This indicates that the pancreas has secreted adequate insulin to allow uptake of the additional glucose by the tissues. In the diabetic individual (with either type of diabetes mellitus), fasting blood glucose level tends to be higher than normal and levels may rise above 11mmol l–1 within thirty minutes of ingesting the glucose drink and remain high for several hours. Effect of exercise in prevention and treatment of non-insulin dependent diabetes mellitus (Type 2) It is known that the ability of the cells to uptake glucose from the blood (insulin sensitivity) is greater in physically fit individuals than in relatively unfit individuals. It is also thought that a decrease in insulin sensitivity with advancing age can be prevented by regular exercise.

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The mechanism for this exercise-induced reduced insulin resistance is thought to be related to adaptations in skeletal muscle, including increased capillary network and blood flow. Enhanced glucose transport due to an increase in the number of insulin receptors on the muscle cell membrane, and increases in the enzymes associated with glucose storage, are also thought to be related to exercise. Improved insulin sensitivity (i.e. reduced insulin resistance) through exercise training starts to be lost within five to seven days of the last bout of exercise, emphasising the importance of regular frequent exercise. General recommendations are the same as for general health – moderate intensity exercise five to seven times a week to be built into the lifestyle. Many epidemiological studies (which look at the occurrence of diseases in large populations) have shown an increase in the incidence of Type 2 diabetes in parts of the world where it was previously uncommon. Heredity cannot account for this large increase over a relatively short time span, and it is more likely to be due to changes in lifestyle – decreased physical activity accompanied by high-energy diets which leads to obesity, a major risk factor for Type 2 diabetes. The relationship between obesity and Type 2 diabetes can be clearly seen in Japanese Sumo wrestlers who are massively obese and must constantly over-eat to maintain their size. The incidence of Type 2 diabetes amongst these wrestlers is reported to be 60% compared with 5% in the general Japanese population. Regular aerobic exercise can play an important role in preventing and/or controlling Type 2 diabetes by reducing body weight, or more importantly, body fat, which in itself reduces many of the risk factors for the Type 2 diabetic. Obese individuals are more at risk of developing Type 2 diabetes and it is believed that 80–90% of overweight Type 2 diabetics can normally achieve metabolic control by following a lowenergy diet combined with a moderate-intensity exercise programme.

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2.4 Osteoporosis Osteoporosis is a long-term condition in which the bones become progressively more porous and brittle, increasing the risk of fractures. The bones become so weak that fractures can occur after only a minor fall, such as when stepping off a kerb. The wrist, spine and hip are the commonest sites of such fractures. Unfortunately, the bone does not break cleanly, as in a typical fracture, but tends to shatter into many fragments which are impossible to reassemble. In such cases, treatment is by surgical replacement of the affected joint with an artificial joint. Other effects of osteoporosis include loss of height, curvature of the spine and chronic back pain (see Figure 34). Figure 34: Height loss caused by osteoporosis.

The disease occurs most commonly in post-menopausal women. Between 20% and 50% of women over 50 are thought to be affected to some extent, while 75% of those over 90 are affected. Men and children may also be affected.

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Bone growth Bone is a living tissue which is constantly renewed throughout life. During childhood and adolescence, bones grow in size. From late adolescence, bones stop growing in length but become increasingly dense. In healthy, physically active individuals with an adequate calcium intake in the diet, peak bone density is reached in the late twenties and early thirties. Thereafter, in females, bone density starts to decline at the rate of about 1% per year, resulting in loss of bone tissue and strength. After the menopause in women, the rate of loss increases to 2–3% per year. In contrast, in men bone density does not decline until over the age of 50, when density decreases at the rate of 0.4% per annum and does not usually cause significant problems until men are in their eighties. Children who consume extra calcium and Vitamin D in the growing years lay down more calcium in their bones than children on less adequate intakes. Ninety-nine percent of the body’s calcium is contained in the skeleton, and when the diet is low in calcium, the body draws on its calcium reserves in the bone to make up the deficit. Therefore, when people reach middle age, those who formed dense bones during their childhood and teens are at an advantage. Hormones and bone growth Between puberty and the menopause, oestrogen maintains bone tissue by stimulating the formation of new bone. The lower levels of oestrogen produced by the post-menopausal woman reduce the activity of bone cells, thereby increasing the risk of calcium loss from the bones. Oestrogen is thought to enhance intestinal calcium absorption and limit its withdrawal from bone, although the exact mechanism of this protective effect is unclear. Men are at relatively low risk of developing osteoporosis as they have larger, stronger bones than women. Risk factors for osteoporosis include: • being elderly • early menopause (under the age of 45) • prolonged absence of periods earlier in life (amenorrhoea)

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• • • • • •

family history of osteoporosis lack of exercise low body fat (fat tissue is a rich source of one type of oestrogen) low calcium intake in diet vitamin D deficiency high alcohol and/or caffeine intake (both promote bone loss).

The effect of exercise in preventing osteoporosis It is known that physically active individuals have a greater bone mass than their less active counterparts of the same age. It appears that regular exercise may help to slow the rate of skeletal ageing, regardless of age or sex. Bone, like muscle, becomes stronger the more it is used and conversely, significant losses in bone density occur when individuals are bed-ridden for any length of time. Astronauts in zero gravity also experience loss of bone density. Bone becomes stronger as a result of the mechanical stress placed on it by the pull of the skeletal muscles in weight bearing exercise. Walking, dancing, jogging, etc. are all thought to increase bone density, while non-weight bearing activities such as swimming are thought to have little effect on bone density. Additional benefits of such exercise include the strengthening of tendons, ligaments and their points of attachments to bones. Therefore, weight bearing exercise should be regarded as essential for the development and maintenance of healthy bones, particularly for women in their twenties and thirties who must maximise bone density before age-related losses occur later in life. Resistance exercise also strengthens bones. This involves moving objects or the body weight to create a resistance – e.g. weight training. Studies of tennis players show a higher bone density in their racquet arms because these encounter much more resistance. In addition to strengthening bones, this type of exercise also helps co-ordination and balance, reducing the risk of falls.

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Exercise in the treatment of osteoporosis There is no cure for osteoporosis but exercise can be used in conjunction with other treatments such as hormone (oestrogen) replacement therapy (HRT) or calcium supplements to halt or even reverse the progress of the disease. For example, forty-five minutes of moderate exercise three times a week not only reduces the rate of calcium loss in older individuals but also stimulates calcium deposition in the bones. However, exercise programmes for individuals with osteoporosis must be carefully designed to avoid the risk of osteoporotic fractures. Walking and activities of moderate intensity can prevent further calcium loss without increasing the risk of fractures. The risks of exercise in female athletes Although exercise is known to be beneficial for bone health, extreme levels of exercise undertaken by some young female athletes may actually cause osteoporosis. When female athletes undergo very intensive training, often combined with a restricted diet, they may reduce their body fat to such a level that the menstrual cycle ceases. This results in reduced levels of oestrogen and loss of its protective effects on bone, making the women more susceptible to calcium loss and reduced bone density. This is particularly serious when it occurs during a period of potential growth, e.g. adolescence. Some studies have found that bone density in some young female athletes is similar to that found in women in their seventies. Unfortunately, these bone losses are thought to be irreversible. This combination of intensive training, restricted diet and low body fat is sometimes referred to as the ‘female athlete’s triad’. Treatment of osteoporosis In summary, osteoporosis is a very common bone disease affecting many people (particularly women) from middle age onwards. Prevention of osteoporosis is far better than any treatment as the agerelated loss of bone mass is not so devastating if the bone mass is well developed before the disease sets in. Weight bearing exercise taken regularly increases the bone mass. This, combined with an adequate

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dietary intake of calcium and vitamin D, are all important in the prevention of osteoporosis. For post-menopausal women, hormone replacement therapy to replace the decreased oestrogen production is often recommended.

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BIBLIOGRAPHY

The bibliography contains full references for all sources used in the preparation of this monograph. Bird S R, Smith A and James K (1998), Exercise Benefits and Prescription, Stanley Thornes (Publishers) Ltd, ISBN 0-7487-3315-9. Chapter 11 of this text provides an excellent review of the current literature on the benefits of exercise for specific conditions. Bodystat Ltd, PO Box 50, Douglas, Isle of Man IM99 1DQ (www.bodystat.com) British Nutrition Foundation website – www.nutrition.org.uk Champe P C and Harvey R A (1994), Lippincott’s Illustrated Reviews – Biochemistry (2nd Edition), Lippincott-Raven Publishers, ISBN 0-39751091-8 Dept of Health (1991), Dietary Reference Values for Food Energy and Nutrients for the United Kingdom. Report on Health and Social Subjects no. 41. London, HMSO, ISBN 0-11-32197-2 McArdle W D, Katch F I and Katch V L (1994), Essentials of Exercise Physiology, Lea and Febiger, ISBN 0-8121-1724-7. This text is highly recommended as additional background reading for this unit. The more advanced texts by the same authors (listed below) are also excellent but somewhat more complex. McArdle W D, Katch F I and Katch V L (1999), Essentials of Exercise Physiology (2nd Edition), Lippincott, Williams and Wilkins, ISBN 0-68330507-7 (new updated edition of above) McArdle W D, Katch F I and Katch V L (1991), Exercise Physiology – Energy, nutrition and human performance (3rd Edition), Lea and Febiger, ISBN 0-8121-1351-9 McArdle W D, Katch F I and Katch V L (1999), Sports and exercise nutrition, Lippincott, Williams and Wilkins, ISBN 0-683-30449-6 McKenna B R and Callander R (1990), Illustrated Physiology (5th Edition), Churchill Livingstone, Edinburgh, ISBN 0-443-04095-8

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Mader, Sylvia (1998), Human Biology (5th Edition), WCB/McGraw-Hill, ISBN 0-697-27821-2 Sizer F and Whitney E (1997), Nutrition Concepts and Controversies (7th Edition), Wadsworth Publishing Co, ISBN 0-314-09635-3 Stalheim-Smith A and Fitch G (1993), Understanding Human Anatomy and Physiology, West Publishing Co, ISBN 0-314-00602-8 Torrance, James (1995), Higher Grade Human Biology, Hodder and Stoughton, ISBN 0-340-63908-3 Tortora G J and Grabowski S R (1993), Principles of Anatomy and Physiology (7th Edition), HarperCollins, ISBN 0-06-046702-9 Vander A J, Sherman J H and Luciano D S (1990), Human Physiology (5th Edition), McGraw-Hill Publishing Co, ISBN 0-07-100998-1 Whitney E N, Cataldo C B and Rolfes S R (1994), Understanding Normal and Clinical Nutrition (4th Edition), West Publishing Co, ISBN 0-314-04178-8

Useful websites Health Education Board for Scotland (HEBS) http://www.hebs.scot.nhs.uk/ British Heart Foundation (BHF) http://www.bhf.org.uk/ Health Education Authority (HEA) http://www.hea.org.uk/ British Nutrition Foundation (BNF) http://www.nutrition.org.uk/

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Adenosine triphosphate (ATP) Compound having a nitrogen base, ribose and three phosphate groups; known as the ‘energy currency’ of the cell. Adrenaline Hormone secreted by the adrenal medulla in times of stress. Angina pectoris Pain in the chest usually resulting from an inadequate blood flow to the heart muscle. Arteries Vessels which carry blood away from the heart. Arterioles Small arteries. Atheroma A mixture of lipid, smooth muscle cells and calcium which develops in the arterial walls in atherosclerosis. Also known as plaque. Atherosclerosis A disease of the arteries in which lipid-containing substances are deposited on the arterial walls, causing a narrowing of their diameters. Atrioventricular (AV) valves Heart valves located between the atria and the ventricles in the heart. Atrium One of the two upper chambers of the heart. Basal metabolic rate (BMR) The rate at which the body uses up energy in the resting, fasted state. Bioelectrical impedance analysis (BIA) A method of estimating body fat by measuring the resistance of the body to the flow of a low-intensity electric current. Blood pressure (BP) The force exerted by the blood against the walls of blood vessels. Body composition The division of the body into fat and fat-free components. Body mass index (BMI) The ratio of body weight to height squared; used as a crude measure of obesity.

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Bomb calorimeter An instrument that measures the heat energy released when foods are burned, thereby providing an estimate of the energy value of the food. Capillaries The smallest type of blood vessels; they connect arterioles with venules and have thin walls only one cell thick to allow substances to enter and leave the blood. Cardiac cycle One complete heart beat, including atrial contraction and relaxation, ventricular contraction and relaxation and the short period when the entire heart is relaxed. Cardiac output (CO) The volume of blood ejected from each ventricle per minute. Cardiovascular disease (CVD) A general term for all the diseases of the heart and blood vessels, including coronary heart disease, atherosclerosis, angina pectoris and stroke. Cardiovascular system (CVS) Body system consisting of the heart and blood vessels. Cerebrovascular accident (CVA) See stroke. Cholesterol A type of lipid that is a component of cell membranes and is used by the body to produce bile and steroid hormones. Coronary arteries Arteries which supply blood to the heart muscle. Coronary heart disease (CHD) A disease of the heart and associated blood vessels supplying the heart. Densitometry A body composition method used to estimate body volume by measuring weight loss when the body is totally submerged under water (underwater weighing). Diabetes mellitus A disease characterised by an abnormally high level of glucose in the blood usually caused by insufficient (Type 1) or relatively inefficient (Type 2) insulin secretion. Diastole Relaxation of a heart chamber; usually refers to relaxation of the ventricles. Diastolic blood pressure (DBP) The lowest pressure exerted by the blood against the arterial walls during relaxation of the ventricles. 68

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Direct calorimetry The measurement of energy expenditure from the heat energy emitted from a body. Echocardiography The use of ultrasound to examine the valves and chambers of the heart. Embolism A blood clot that breaks loose from accumulated matter in the blood vessels and travels through the circulatory system. Energy balance The state when energy intake is equal to energy output and body fat stores are constant. Fat-free mass (FFM) All fat-free chemicals and tissues in the body including water, muscle, bone and connective tissue. Fat mass (FM) All chemical fat in the body. Glucagon A hormone secreted by endocrine cells in the pancreas that increases blood glucose. Glucose tolerance test A blood test used for the diagnosis of diabetes mellitus; measures the blood glucose levels over several hours in response to a glucose drink. Glucosuria Abnormally high amount of glucose in the urine. Heart rate (HR) The number of heart contractions per minute. High-density lipoprotein (HDL) The type of lipoprotein that transports cholesterol back to the liver from the peripheral cells; known as ‘good cholesterol’. Hyperglycaemia Abnormally high levels of blood glucose. Hypertension High blood pressure. Hypoglycaemia Abnormally low levels of blood glucose. Hypotension Low blood pressure. IDDM Insulin-dependent diabetes mellitus; less common type of diabetes occurring mainly in young people, caused by lack of insulin brought on by damage to insulin-producing cells in the pancreas. Also known as Type 1 diabetes or early-onset diabetes.

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Indirect calorimetry Estimation of energy expenditure from measurement of the amount of oxygen used by the body. Insulin A hormone secreted by endocrine cells in the pancreas which decreases blood glucose by increasing cellular uptake of glucose. Insulin resistance Condition in which cells become less responsive to insulin; they cannot take up as much glucose despite adequate insulin production. Ischaemia Lack of oxygen (usually temporary) caused by a decreased blood flow to a group of cells or tissues. Islets of Langerhans Clusters of endocrine cells in the pancreas which secrete insulin (β cells) and glucagon (α cells). Kilocalorie (kcal) Unit of energy defined as the amount of energy required to raise the temperature of 1 kg of water by 1 degree Celsius. Kilojoule (kJ) The SI unit for the measurement of energy (1 kcal = 4.18 kJ). Low-density lipoprotein (LDL) The major carrier of cholesterol, transporting it from the liver to the tissues where it is used in cell membranes and for steroid hormone synthesis. Known as ‘bad cholesterol’ as high blood levels of LDL are strongly linked with increased risk of heart disease. Myocardial infarction (MI) Damage to the heart muscle caused by blockage of the coronary arteries. Commonly referred to as a ‘heart attack’. Negative feedback A type of control in which a stimulus (e.g increase in body temperature) initiates actions which reverse that stimulus (i.e. reduce body temperature). NIDDM Non-insulin dependent diabetes mellitus; commoner type of diabetes occurring mainly in individuals over 40, resulting from a loss of tissue responsiveness to insulin. Also known as Type 2 or late-onset diabetes. Obesity A disease characterised by excessively high body fat in relation to lean body tissue.

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Osteoporosis A condition characterised by a reduction in bone density leaving bones brittle and fragile; commonly seen in post-menopausal women and elderly men. Peak bone density The highest attainable bone density for an individual; developed during the first three decades of life. Physical activity ratio (PAR) The energy cost of an activity expressed as a multiple of the BMR; e.g. PAR for ‘walking at average speed ‘ is 2.8 × BMR. Platelets Cell fragments found in blood that function in the clotting process. Plaque See atheroma. Pulmonary circuit Short circulatory loop carrying deoxygenated blood from the right ventricle to the lungs and returning oxygenated blood from the lungs to the left atrium. Semi-lunar valves Valves which lie between the aorta and the left ventricle and between the pulmonary artery and the right ventricle. Sphygmomanometer An instrument for measuring arterial blood pressure. Stroke Destruction of the brain tissue resulting from blockage of blood vessels which supply the brain. Also known as a cerebrovascular accident (CVA). Stroke volume (SV) The volume of blood ejected by a ventricle per beat. Systemic circuit System of blood vessels which carry oxygenated blood from the left ventricle to all the organs of the body and return deoxygenated blood to the right atrium. Systole In the cardiac cycle, the phase of contraction of the atria or ventricles. Systolic blood pressure (SBP) The highest pressure exerted by blood against the walls of the arteries during ventricular contraction; about 120 mm Hg under resting conditions for a young healthy adult.

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Thermic effect of food (TEF) The energy required to digest, absorb, metabolise and store food. Thrombosis The formation of a blood clot in a blood vessel; e.g. coronary thrombosis – blockage of a coronary artery by a blood clot resulting in a myocardial infarction or heart attack. Thrombus A blood clot which may obstruct a blood vessel or the heart cavity. Total peripheral resistance (TPR) The sum of all resistances of all systemic blood vessels. Type 1 diabetes See IDDM. Type 2 diabetes See NIDDM. Vasoconstriction A narrowing of a blood vessel caused by contraction of the smooth muscle lining the vessel. Vasodilation The widening of a blood vessel caused by relaxation of the smooth muscle lining the vessel. Veins Blood vessels which carry blood from the tissues back to the heart. Ventricles The two larger, lower heart chambers. Venules Small veins that collect blood from capillaries and deliver it to veins. ° A measure of the maximum amount of oxygen that a person can VO 2max utilise; used as a measure of aerobic fitness.

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Physiology helath and Exercise (Part 2)