Physiology helath and Exercise (Part 2)

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SECTION 1

1.1 Structure and function of the cardiovascular system

The cardiovascular system consists of a double pump (the heart) and asystem of blood vessels to transport the blood around the body.

In the healthy individual, the cardiovascular system works veryefficiently, but it is subject to several degenerative changes (someavoidable, some unavoidable) such as atherosclerosis, which may resultin the development of cardiovascular disease (CVD) particularlycoronary heart disease (CHD) which may ultimately result in a heartattack (myocardial infarction – MI).

Before examining the pathophysiology of cardiovascular disease, wemust 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. Thelargest arteries (e.g. the aorta) have thick, elastic walls which canstretch to accommodate the surge of blood after each contraction ofthe heart. Arteries branch many times, forming smaller and smallervessels, the smallest of which are arterioles. Contraction of thesmooth muscle lining the walls of the arterioles allows them to openor close to varying degrees to adjust blood flow to different parts ofthe body. For example, when we are faced with danger, arterioles inthe skeletal muscles dilate, which increases the blood flow (andtherefore the oxygen supply), allowing us to flee or face the dangerhead on. (This is part of the ‘fight or flight’ response.) At the sametime arterioles in the digestive system constrict, reducing blood flowto the gut and increasing the blood available to the muscles.

• Capillaries are tiny vessels where the exchange of substances withthe tissues occurs. Their walls are only one cell thick, allowingnutrients and waste to pass through with ease. They form extensivebranching networks (capillary beds) throughout the body tissues, butonly certain beds are open at any one time. This allows the shuntingof blood from one region to another.

• Veins (and venules) carry blood back to the heart. Blood flows out ofthe capillaries into the smallest of the veins – venules – which in turnre-unite to form larger veins. The walls of veins are thinner thanarteries and often have valves to prevent backflow of blood.

EXERCISE AND THE CARDIOVASCULAR SYSTEM (CVS)

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Figure 1: Blood vessels.A: oxygenated blood leaves the heart from the left ventricle via theaorta, moves through arteries to arterioles to capilleries to venules andreturns to the right atrium by way of veins;B: arteries have well developed walls with a thick middle layer ofelastic tissue and smooth muscle;C: capillary walls are one cell thick;D: veins have thinner walls than arteries (with less elastic tissue andsmooth muscle), and have valves that prevent the backflow of blood.

The heart

This muscular, fist-sized organ, which lies between the lungs behind thesternum (breastbone), is a double pump consisting of four chambers –two upper, thin-walled atria and two lower, thick-walled ventricles. Theleft ventricular wall is thicker than that of the right ventricle as it has topump blood all round the body, while the right ventricle only pumpsblood to the lungs.

The cardiovascular system consists of two distinct circuits:

• The pulmonary circuit carries deoxygenated blood from the rightventricle to the lungs via the pulmonary arteries and returnsoxygenated blood to the left atrium of the heart via the pulmonaryveins. (Note that the pulmonary arteries are the only arteries thatcarry deoxygenated blood.)


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• The systemic circuit carries oxygenated blood to the rest of thebody, starting from the left ventricle, which pumps blood into theaorta. The aorta branches into many arteries, which in turn transportblood to other organs and major body regions. The deoxygenatedblood is returned by the veins to the right atrium.

Figure 2 illustrates the path taken by the blood through the circulatorysystem.

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 andprevent backflow of blood.

Those lying between the atria and the ventricles are known asatrioventricular (AV) valves.

The semi-lunar (half-moon) valves lie between the left ventricle and theaorta and the right ventricle and the pulmonary artery.

The heart sounds heard through a stethoscope (‘lub-dub’) are actuallythe 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 closingproperly.

The cardiac cycle

Each heartbeat is called a cardiac cycle and consists of the followingsequence 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 byventricular contraction);

• diastole – relaxation of the heart.

At rest, the heart contracts or beats about 72 times a minute (normalrange 60–90) and each cardiac cycle lasts about 0.8 seconds (0.3 secondsfor systole; 0.5 seconds for diastole).

Figure 3 shows a diagrammatic representation of the sequence of eventsduring one cardiac cycle.


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Figure 3: The cardiac cycle. The sequence of events during a singleheart beat. The whole cycle takes about 0.8 seconds at a heart rate of 72beats per minute.

The surge of blood entering the arteries during systole stretches theirelastic walls, which then recoil during diastole, thus maintaining bloodflow when the heart is relaxed. This alternating expansion and recoil ofthe arteries can be felt as a pulse at several arteries in the body, e.g. theradial 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 ventricleper minute and is the function of two factors – heart rate (HR) (beats/min) and stroke volume (SV) which is the volume of blood ejected byeach ventricle during each contraction.

CO = HR × SV

At rest: HR = 72 beats/min; SV = 70 mli.e. CO = 72 × 70 = 5040ml/min

= 5 litres/min


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Cardiac output varies between individuals and depends on their physicalfitness and level of activity. For example, the heart of a highly trainedathlete can pump 30–35 l/min while most non-athletes can only achievea maximum cardiac output of about 20 l/min.

Table 1 below shows some typical values for cardiac output at varyinglevels of activity.

Activity Heart rate Stroke volume Cardiac outputlevel (HR) (SV) (l/min)

(beats/min) (ml) (HR ××××× SV)

Rest 72 70 5

Mild 100 110 11

Moderate 120 112 13.4

Heavy (highlytrained athletes) 200 150 30

As the work load increases, HR increases to a maximal value of about180–200 beats/min (220 minus age in years) while SV increasesproportionately less (70–150 ml). The increase in cardiac output withexercise is achieved principally by increasing the heart rate.

Blood pressure (BP)

The force exerted by the blood against the walls of the blood vessels isknown as the blood pressure. It is highest in the large elastic arteries,gradually dropping as it travels round the circulatory system and isalmost zero by the time it returns to the right atrium. (Low BP in thecapillaries allows the efficient exchange of substances between the bloodand 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) andlowest during relaxation of the ventricles (diastolic BP).

Both systolic and diastolic BP can be measured by an inflatableinstrument called a sphygmomanometer which is wrapped around theupper arm (see Figure 5). A stethoscope is placed over the brachialartery just below the cuff and the cuff is inflated until the pressure stopsthe flow of blood through the artery. The air in the cuff is then graduallyreleased. When the pressure in the artery exceeds the pressure in thecuff the blood starts spurting through the artery again and can be heardthrough the stethoscope and felt by the subject as a pulse. The pressureat which this occurs is the systolic BP. As more air is released from thecuff, the sounds get louder as blood flow becomes more turbulent, andthen become muffled and finally disappear. The pressure at which thishappens is the diastolic BP and is the point when blood is flowingcontinuously through the artery.


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Figure 5: Measuring blood pressure at the brachial artery using asphygmomanometer.

The pressure is measured in millimetres of mercury (mm Hg) and atypical reading for a young healthy adult is about 120/70 mm Hg (SBP/DBP) although readings vary considerably within the normal range fromone person to the next and fluctuate throughout the day.

As a person ages, BP tends to rise due to atherosclerosis and so areasonably healthy 65-year-old may have a resting BP of 140/90 (referredto as 140 over 90).

Hypertension or high blood pressure is prolonged elevation in BP oftendue to ‘hardening of the arteries’ caused by the deposition of calciumand fatty substances in the arterial linings. Other causes include kidneydisease; high salt intake; obesity, and genetic predisposition.

Systolic BP may increase to 300 mm Hg and diastolic BP may exceed 120mm Hg. Although hypertension can be symptomless in the early stages,it ultimately puts an excessive strain on the heart and, if untreated, willeventually 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 inhealthy individuals, but what can go wrong with the system?

Cardiovascular disease (CVD), which refers to diseases of the heart andblood vessels, is the major cause of death in men and women over 50 inthe western world. In the UK, 350,000 people die from CVD every year.It includes diseases such as coronary heart disease (CHD) which itselfincludes angina pectoris, myocardial infarction and sudden death andstroke. The UK, particularly Scotland, has the unenviable distinction ofbeing near the top of the international league for death from CHD.

Atherosclerosis and hypertension are the two disease processes that leadto most cases of CVD.

Atherosclerosis

Atherosclerosis is the accumulation of a material known as atheroma orplaque beneath the inner lining of the arteries. (Atheroma is the ancientGreek word for porridge, and the material is so called because thedeposits look like blobs of porridge.)

The process starts with the build up of fatty material (mainlycholesterol), but as the disease progresses, fibrous material and calciumalso 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 thearteries) 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 ofplaque narrows the diameter, obstructing and eventually blocking theflow of blood.

Contributing factors to the development of atherosclerosis are highblood pressure, carbon monoxide in cigarettes, diabetes mellitus andhigh blood cholesterol levels.

The condition can affect any artery, but the consequences areparticularly serious when it affects the coronary arteries, the arteriessupplying the heart muscle.

Although atherosclerosis develops progressively from early to middleage, symptoms do not tend to arise until the age of 50 or over, that isuntil the coronary arteries are markedly narrowed or until a clot orthrombus blocks the artery.

Thrombosis

The plaque provides a roughened surface that allows blood platelets toaccumulate. The platelets release clotting factors which may result in theformation of a blood clot or thrombus at the site of plaque formation. Ifthe thrombus grows large enough to obstruct the artery completely, athrombosis occurs. For example, a coronary thrombosis closes off one ofthe blood vessels supplying the heart, while a cerebral thrombosis closesoff a blood vessel in the brain.


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If the thrombus breaks loose from the site of formation (now known asan embolus), it travels along the blood stream until it reaches an arterytoo narrow to allow it to get through.

If this embolism occurs in a coronary artery, the part of the heartsupplied by the artery will be deprived of oxygen and die – a heartattack or myocardial infarction (MI) results. The consequences of an MIdepend on the area of the heart muscle affected – if a very tiny branch ofthe coronary artery is affected, the MI may go unnoticed (silentinfarction), whereas blockage of a larger branch will cause severe chestpains and is often fatal.

Figure 7 illustrates how the build-up of atheroma eventually leads to anMI in the coronary arteries.

Figure 7: The build-up of atheroma in coronary arteries, thateventually 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 thearea of brain tissue destroyed.

Angina pectoris

Angina pectoris is chest pain brought on by anything that makes theheart work harder, such as exercise, excitement, emotional upset. Itarises when the blood flow through the coronary arteries is reduced byatherosclerosis.

At rest, the blood flow and therefore oxygen supply to the heart muscleis usually adequate, despite narrowing of the arteries. However, whenthe heart needs to work harder, during exercise for example, therestricted blood flow may not be able to meet the additional oxygenrequirements of the heart muscle. Unlike skeletal muscle, cardiac musclecannot work anaerobically (without oxygen), and the resulting lack ofoxygen causes the ischaemic pain of angina pectoris, which disappearsafter a short period of rest.

Angina symptoms tend to appear only when atherosclerosis is quiteadvanced, with the diameter of the coronary arteries reduced by about70%.

Hypertension

As previously stated, hypertension is defined as a persistently highresting 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 definedas in Table 2 below.

Hypertension Diastolic BP(mm Hg)

Mild 85 – 89

Moderate 90 – 104

Moderately high 105 – 114

Severe Greater than 115


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It may be caused by constriction of the arteries due to atherosclerosisand/or loss of elasticity of the arterial walls.

Hypertension is a major risk factor for many diseases, includingcoronary heart disease. Contributing factors include diet (high salt, highfat), 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 membranesand the precursor for the synthesis of all steroid hormones such astestosterone, oestrogen and progesterone, and bile salts which areessential 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. Ifthe diet contains a lot of cholesterol, the liver compensates by makingless, and similarly it makes more if the diet does not contain enoughcholesterol (less likely).

More important than the amount of cholesterol in the diet is the type offat eaten. When saturated animal fats are broken down in the body, theliver 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 bloodare more likely to develop CHD than those with lower levels.

There are two important types of cholesterol-carrying proteins in theblood known as low-density lipoproteins (LDL) or ‘bad’ cholesterol andhigh-density lipoproteins (HDL) or ‘good’ cholesterol.

LDL carries about 60–70% of total blood cholesterol and its function isto deliver cholesterol from the liver to the body cells for membrane andhormone synthesis. Under abnormal conditions cholesterol is alsodeposited 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 gatheror scavenge cholesterol from body cells and transport it back to the liverfor elimination or use in the production of bile salts. As blood levels ofHDL increase, the risk of CHD decreases.


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The risk of developing CHD may be predicted by measuring the ratio ofHDL to LDL in the blood.

A high ratio indicates that HDL level is high and LDL level is low whichgenerally is healthy, while a low ratio indicates low HDL levels and highLDL levels which is generally unhealthy. There is some evidence tosuggest that levels of HDL can be increased by exercise.

Total plasma cholesterol can be measured very quickly (in about threeminutes) by a simple fingerprick test, but information about theHDL: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 indeveloped countries over the last twenty to thirty years, CHD is still theleading cause of death.

Physical inactivity has been identified as an independent risk factor forCHD which may aggravate the classical risk factors of smoking, highblood cholesterol and hypertension.

The actual mechanisms by which physical activity affects health are stillunclear and are the subject of much research, but findings to datehighlight the benefits of physical activity both in the prevention of manydiseases and also in the treatment of individuals with known CVD –cardiac rehabilitation exercise programmes are known to be importantwith 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 thesupposed benefits of physical activity with regard to cardiovascularhealth, we must understand how the healthy cardiovascular systemresponds 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 ofoxygen and nutrients to the exercising muscles and also remove wasteproducts 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) andstroke volume (SV), both of which increase in proportion to theintensity of exercise. For example, in a relatively untrained person, HRmay increase from 70–170 beats/minute and SV from 70 ml to 120 mlper beat, giving an increase in CO from 5 litres per minute at rest toabout 20 litres per minute.

These changes are caused by:

• increased output from sympathetic nerves to the heart whichincreases HR;

• increased release of adrenaline into the blood which increases HRand SV;

• increase in blood volume returning to the heart which increases therate of filling of the heart chambers. This causes stretching of theventricular walls which respond by contracting more forcibly so thatmore blood is ejected with each contraction, i.e. SV is increased. Themore the ventricular walls are stretched, the greater the force ofcontraction.

The athlete’s heart

Why do endurance athletes have lower heart rates both at rest and atany given level of exercise?

Endurance training can reduce resting heart rates to as low as 30–40beats per minute. Like skeletal muscle, cardiac muscle is strengthenedby training and is capable of more forceful contraction which increasesthe stroke volume and, as a result, the heart of an endurance athlete hasa considerably larger SV at rest and during exercise than an untrainedindividual of the same age.


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When comparing the CO during maximal exercise in trained anduntrained individuals (Table 3), it can be seen that the enduranceathlete achieves a larger CO mainly because of a relatively greaterincrease in SV.

Table 3: Comparison of maximal CO in trained and untrainedindividuals

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 theheart. There is an increase in protein synthesis leading to thickening ofindividual muscle fibres, and an increase in the number of contractileelements 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 anormal response to endurance training.

This increase in size is temporary, however, and the heart returns to itspre-training size if intensity of training decreases.

Echocardiography has provided a better understanding of the changesin the dimensions of the heart with training. Sound waves are passedthrough the heart which can measure the size of the cardiac muscle andthe volumes of the chambers (Table 4).

Table 4: Comparison of left ventricular mass and volume in trainedand 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 exercisingmuscles to supply them with oxygen and nutrients, and a decreasedblood 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 supplyingthe active muscles and vasoconstriction (narrowing) of arteriolessupplying regions such as the gut and kidneys.

For example, Figure 8 shows that, at rest, renal blood flow accounts forabout 20% of the total CO of 5.8 l (i.e. 1100 ml/min), while duringmaximal 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 duringstrenuous exercise about 70% of CO goes to skeletal muscles.

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


Strenuousexercise(ml/min)

Rest(ml/min)

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Total

750

750

250

1200

500

1100

1400

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5800

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12,500

1900

600

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17,500

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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 thecombined effects of increased CO (which would tend to increase BP)and a general vasodilation of arterioles to exercising muscles (whichwould tend to decrease BP). The overall reduction in total peripheralresistance to the flow of blood caused by the latter largely offsets theincrease in CO, allowing increased delivery of oxygen and nutrients tothe working muscles without causing a substantial increase in BP whichcould damage blood vessels and other organs.

Figure 9: Changes in systolic, diastolic and mean arterial bloodpressures with increasing intensity of exercise.

Exercise and hypertension

Many studies have shown that regular prolonged aerobic exercise iseffective in causing moderate decreases in BP both at rest and duringexercise.

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 bloodflow and subsequent decrease in BP

• exercise which may facilitate elimination of sodium by the kidneysresulting in a decreased fluid volume and BP.


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With increasing age, arteries tend to lose their elasticity, which causes aslight increase in BP. However, it is thought that this loss of elasticitymay be largely prevented by regular aerobic exercise throughout life.

Exercise also has acute effects on BP. After a bout of exercise, forexample, resting BP falls below pre-exercise levels. This post-exercisehypotension is thought to have important long-term consequences bothin the prevention and treatment of high BP, if exercise is repeatedregularly.

Principles of exercise testing

There are many reasons why it may be necessary to assess thephysiological fitness of an individual, whether an athlete in training or apatient recovering from a myocardial infarction or heart surgery.

An exercise test can provide baseline data against which laterassessments 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 physicalcondition 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 theirability to use oxygen, and this depends on the efficiency of theircardiovascular and respiratory systems in delivering oxygen to theexercising muscles at the required rate.

A measure of the maximum amount of oxygen that a person can utiliseis called the maximal oxygen uptake or VO

2max. The higher the value of

the VO2max

, the greater the aerobic fitness of the individual.

This test, which uses sophisticated laboratory apparatus to measureoxygen consumption and carbon dioxide production, requires theparticipant to exercise to exhaustion and is therefore only suitable forevaluating the fitness of competitive athletes.


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Table 5: Typical values for VO2max

Group (25–35 years) VO2max(ml/kg/min) VO2max(ml/kg/min)Men Women

Elite endurance athletes 70–80 60–70

Highly trained teamgames 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 furtherincrease in oxygen consumption despite an increased workload (seeFigure 10).

Figure 10: Graph showing oxygen consumption against work intensity,and that illustrates the plateau in consumption despite anincreasing workload.

As already stated, VO2max

testing is not suitable for most individuals andhas several limitations – it requires expensive laboratory equipment,highly trained technical personnel, and medical back-up.

For these reasons, several less complex indirect measures of VO2max havebeen developed which require the individual to exercise at much lower


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Plateau in oxygen consumption

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intensities. These predictive tests are known as sub-maximal tests. Theyare based on the assumption that there is a direct linear relationshipbetween heart rate, oxygen consumption and intensity of exercise.

By measuring heart rate and oxygen consumption at several levels ofwork intensity, it is possible to predict VO2max by extrapolating to theirpredicted maximum heart rate calculated from 220 minus age in years.

There are however some important possible sources of error in thispredicted VO

2max :

• Heart rate (especially at low levels) can be affected by other factorsapart from exercise, such as emotion, previous meal, temperature,anxiety, etc.

• Predicted maximum heart rate may not be accurate for a particularindividual.

Figure 11 shows how a sub-maximal test may be used to monitorchanges in aerobic capacity before and after a training programme.

Figure 11: Prediction of VO2max before and after training byextrapolating the linear relationship between heart rate and oxygenuptake during graded exercise.


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Oxygen uptake (litres/min)

Assumed max. HR

Before training

After trainingPredicted Vo2max

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Exercise stress tests

Often, individuals with chronic CHD will exhibit normalelectrocardiogram (ECG) traces at rest but abnormal ECGs duringexercise. Such individuals undergo stress tests on a treadmill whenworkload is increased in an incremental fashion whilst their ECG isclosely monitored. An example of one of the most commonly usedprotocols, the Bruce Protocol, is shown in Figure 12.

Figure 12: Illustration of the Bruce Protocol, an example of a stress testused 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 toevaluate the efficiency of the cardiovascular response to exercise.

There are many different protocols for step tests but all are based on thesame physiological principles.

They involve the subject stepping up and down from a step or bench ata fixed pace for several minutes (3–5 minutes). The height of the stepand the rate of stepping (often set by a metronome) vary with differentprotocols.

At the end of the exercise, HR is measured for 15–30 seconds at one-minute intervals for about four minutes after cessation of exercise tomeasure the rate of recovery.


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The fitter the individual, the lower the HR will be immediately afterexercise and the faster it will return to its resting level.

Figure 13 shows the heart rate response during a stepping exercise andin recovery for three individuals of varying levels of fitness, Subject Abeing the fittest and Subject C the least fit.

Figure 13: Heart rate response during a step test and in recovery forthree individuals of different levels of cardiovascular fitness.

It is also possible to measure heart rate continuously during exercise bywearing an HR monitor.

An identical test can be repeated at a later stage in order to evaluate anychanges in the aerobic fitness, with lower HRs indicating animprovement 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 formoderately fit individuals.

Participants run between two markers positioned twenty metres apart ata pace determined by a pre-recorded tape. The test starts at a fairly slowpace which increases every minute and the individual runs between thetwo markers until they cannot keep up with the pace. The level theyreach (i.e. number of completed shuttles) is recorded and may be usedto predict VO2max.

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A variation of this test – the shuttle walking test – is more suitable forless fit individuals.

Role of exercise in cardiac rehabilitation

Over the last twenty years there has been a major change in thetreatment of patients who have had a heart attack or who haveundergone cardiac surgery.

Before the 1970s, complete bed rest for at least six weeks following aheart attack or surgery was the standard treatment. This was to allowtime for the damaged heart muscle to form scar tissue.

Now, however, some form of supervised aerobic exercise sessions areincluded in all cardiac rehabilitation programmes, which also offeradvice 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 atwhich they can cope with the physical demands of everyday life.

The initial stages of the exercise programme are likely to start within aweek 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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2.1 Energy

The need for energy

Energy is needed for:

• the basal requirements which keep the body alive – i.e. energy forkeeping the heart beating, for breathing, for maintaining bodytemperature and all the other vital processes. This is known as theBasal Metabolic Rate (BMR);

• active movement – i.e. muscle contraction;

• synthesis of enzymes and other cellular materials, to allow growthand repair of body tissues;

• pregnancy and lactation.

Energy comes from the food we eat. The stored chemical energy incarbohydrates, fats, and proteins is released by the series of biochemicalreactions 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 energyexpended by the body, the individual is in energy balance.

When the diet provides more energy than the body is using, the excessenergy is stored as body fat and the individual gains weight – a positiveenergy 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 willlose weight – a negative energy balance.

Figure 14 illustrates the principle of energy balance.

EXERCISE AND METABOLISM

SECTION 2

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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 (1000calories = 1 kcal) and this term is still widely used both by nutritionistsand the general public particularly with reference to food labelling andweight-reducing diets. For this reason, it is important to be familiar withboth terms.

1 kcal = 4.18 kJ


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Energy is provided mainly by three nutrients found in food –carbohydrate, fat and protein. Alcohol (which is not a nutrient) alsoprovides energy.

Carbohydrate: 16 kJ per gramFat: 37 kJ per gramProtein: 17 kJ per gramAlcohol: 29 kJ per gram

The amount of energy provided by the diet depends on the proportionsof carbohydrate, fat, protein and alcohol that are present – e.g., a high-fat diet will provide more energy than a low-fat diet.

To find out how much energy a particular food provides, the food isburnt in a bomb calorimeter (Figure 15). This breaks the chemical bondsholding the atoms together resulting in the release of heat energy whichcan be measured.

Figure 15: The bomb calorimeter.

Published tables and computerised dietary analysis programmes havebeen designed to calculate an individual’s total energy intake.

The amount of energy required by an individual depends on three mainfactors:

• 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 constantover a period of time), energy requirements can be gauged accuratelyeither by measuring the total amount of energy consumed or measuringthe total energy expenditure of the individual over several days. Bothtechniques can be time-consuming and costly and require highlymotivated subjects. However, the average energy requirements can beestimated from published tables.

In the UK, the Department of Health published Estimated AverageRequirements (EAR) per day for energy for various age/sex groupswithin the population. For example:

Table 6

Age (years) Estimated Average Estimated AverageRequirement (males) 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 istrue for the majority of individuals in the UK.

These estimated energy requirements are useful for studies of largegroups of people but should only be used as a guide when consideringan individual, whose energy requirements may be considerably more orless than the estimated value.

Dietary recommendations for health

A small positive energy balance over a long period of time will lead tobeing overweight and eventually to obesity, which is an important riskfactor in the development of coronary heart disease, high bloodpressure, stroke and Type 2 diabetes mellitus.

There has been a marked increase in the prevalence of obesity in the UKin the past fifty years and particularly in the last ten to twenty years.


BIOLOGY 2 9

There are many possible reasons for this, the most likely being:

• a marked reduction in the level of physical activity both at work andduring leisure time (e.g. increased use of cars; increased time spentwatching television and playing computer games);

• the percentage contribution from energy-dense fat in the diet isrelatively high (about 38%) despite an overall decrease in the averagetotal energy intake.

Figure 16 shows the percentage contribution of protein, fat andcarbohydrate to the average British diet in 1995, while Figure 17illustrates the changing proportions of these nutrients to total energyintake since 1943.

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


Protein 15%

Total fat 38%

Total carbohydrate 47%

Average energy intakeper person per day= 7800 kilojoules1kcal = 4.18kJ

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Figure 17: Changes in energy intake from protein, fat andcarbohydrate, 1943-1992. (Source: MAFF Household Food Consumptionand Expenditure 1990, HMSO, 1991 and MAFF National Food Survey1992, HMSO, 1993).

In order to reduce the high prevalence of obesity, heart disease, etc. inthe UK, the recommendations are to reduce the contribution from fatfrom 38% to 35% and eventually to 30%, while increasing thecontribution from complex carbohydrates (i.e. cereals, starches, etc.)from 47% to about 50% of total energy consumed.


0 20 40 60 80 100

Percentage of energy

1943*

1952

1962

1972

1982

1992

Year

*Records begin

Fat Carbohydrate Protein

BIOLOGY 3 1

Energy expenditure and its measurement

The total amount of energy expended by the body is the sum of threecomponents:

1. Basal metabolic rate,2. Thermic effect of food,3. Physical activity.

1. Basal metabolic rate (BMR)

This is the energy expended in the resting, fasting state and is theenergy required to carry out normal body functions such as breathing,circulation of blood, etc. It is the energy that would be used by a personsimply lying in bed all day.

It is the largest component of an average individual’s energyexpenditure and in sedentary adults accounts for about 60–70% of totalenergy 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, themore energy is expended.

However, even at a given body weight, BMR can differ greatly betweenindividuals due to differences in their body composition – i.e therelative proportion of lean to fat tissue. Lean tissue (e.g. muscle) is moremetabolically active than fat (adipose) tissue, therefore the greater theproportion of lean tissue an individual has, the higher their BMR. Forexample, if two individuals of the same weight, height, age and sex arecompared, the one with the greater amount of lean tissue is likely tohave the higher BMR.

(b) Age

BMR per kg body weight is higher in children owing to the energy costof growth, but from 18–20 years, BMR per kg decreases at the rate ofabout 2% per decade.

This age-related fall is partly due to changing body composition as weget 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 higherproportion of lean tissue. For example, the average % of body fat for a20-year-old 60-kg male is about 12–15%, and he is likely to have a higherBMR than a 20-year-old 60-kg female, who is likely to have average bodyfat of 25–30%.

(d) Nutritional status

BMR is reduced by fasting or by being on a very low-energy intake forany 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 energybalance.

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 reasonsfor the failure of many weight-reduction diets. The body adapts to thelower food intake, so in order to keep losing weight, food intake mustbe 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 acomfortable environment (not too hot or too cold); free from anxiety;etc.

Alternatively, there are a number of age-, weight- and sex-adjustedequations for the prediction of BMR when an actual measurement is notpossible.

Examples of some of these equations are shown below:

Males

10–17 years: BMR (MJ/d) = 0.074 × body weight (kg) + 2.75418–29 years: BMR (MJ/d) = 0.063 × body weight (kg) + 2.896


BIOLOGY 3 3

Females

10–17 years: BMR (MJ/d) = 0.056 × body weight (kg) + 2.89818–29 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 storeingested nutrients. Depending on the quantity and composition of thefood eaten, energy expenditure may increase as much as 30% abovebasal in the two to three hours following a meal. Over a twenty-four-hour period, the thermic effect of food accounts for about 10% of thetotal energy expended.

The thermic response to a meal can vary considerably depending on thequantity and type of food eaten. For example, the thermic response canvary 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 fora high-fat meal.

This means that people on a high-fat diet will not use up so muchenergy to digest and absorb their food as someone on a healthier high-carbohydrate diet. This highlights one of the many dangers of high-fatdiets.

3. Physical activity

This is the energy expended above resting to move about and performtasks 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 sedentaryindividuals, up to more than 50% in those engaged in heavy manualwork or vigorous training programmes.

Table 7 shows some typical values of the energy cost of various activities.


BIOLOGY3 4

Table 7

Activity Body wt = 55 kg Body wt = 80 kgkJ/ min 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-countryski-ing 54.3 76

Note that a heavier person usually uses up more energy to perform anactivity 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


BIOLOGY 3 5

Physical activity is the biggest single component of the total energyexpenditure which can be changed voluntarily, and is likely to be themain reason for individual differences in energy requirements. Theenergy expended in physical activity is largely determined by occupationand leisure activities.

The energy required for physical activity of any kind depends on severalvariables, such as the intensity and the duration of the activity and themuscle masses involved. When considering the influence of physicalactivity on energy expenditure, it is important to distinguish betweenshort bursts of strenuous activity and moderate activity of relatively longduration. For example, a thirty-minute game of squash at 42 kJ/minwould use 1260 kJ whereas a three-hour round of golf at 16.7 kJ/minwould use 3010 kJ.

Energy expenditure (EE) does not return to baseline values immediatelyafter the activity stops. The size of this post-exercise elevation of EEdepends on the intensity of the exercise. If exercise is severe, EEremains elevated above resting levels for some time after the activity hasstopped.

This metabolic response is known as excess post-exercise oxygenconsumption (EPOC) and is due to the need for oxygen to replenishglycogen 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 toforty minutes of cessation of exercise, and accounts for only about20–100 additional kJ expended. Although this is a small amount in termsof total energy expended, it has the potential to help maintain energybalance if exercise is undertaken on a regular basis.

Several studies have suggested that exercise may increase BMR – and asthis increase is lost after several days of inactivity, regular exercisepatterns are important.


BIOLOGY3 6

Measurement of energy expenditure (EE)

There are several methods of measuring EE. The most commonly usedones are:

1. Direct calorimetry

All of the energy produced by the body’s metabolic reactions ultimatelyresult in heat production. Therefore measurement of the heatproduced by the body gives a measure of energy released.

Under laboratory conditions, heat production can be measured in aspecially designed, airtight chamber called a direct calorimeter, in whicha person can live for several days (see Figure 18).

Figure 18: The direct calorimeter.

Heat production is measured by temperature changes in water flowingthrough a series of pipes at the top of the chamber.

As the chamber is heavily insulated, any change in water temperaturemust be due to heat produced and radiated by the individual. Oxygen iscirculated through the chamber, and exhaled air is passed throughchemicals which remove water vapour and carbon dioxide.

This very accurate technique has been used extensively over many yearsfor research purposes, but is unfortunately very expensive andtechnically difficult to operate, making it unsuitable for large-scalestudies of free-living individuals.


BIOLOGY 3 7

2. Indirect calorimetry

Since 95% of energy production in the body depends on the presence ofoxygen, it follows that the measurement of the oxygen consumed by thebody over a period of time gives an indirect measure of energyexpenditure. This is known as indirect calorimetry.

Compared to direct calorimetry, this technique is much simpler and lesscostly but is also highly accurate if carried out carefully.

The subject breathes in air which has a known and constant compositionof 20.93% oxygen, 0.03% carbon dioxide and 79.04% nitrogen. The airbreathed out by the subject will have less oxygen (usually 16–18%) andmore carbon dioxide (3–5%).

Measurement of oxygen consumption by the body requires knowledgeof 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 forten to fifteen minutes in a large plastic bag. A small sample of theexpired air is analysed for its oxygen and carbon dioxide content, andthe total volume of air expired is measured by a gas meter.

The following example illustrates how oxygen consumption can becalculated. (For ease of calculation, it is assumed that % oxygen ininspired air is 21%.)

Example

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

Volume of O2 in inspired air = 21% of 100 l = 21 lVolume of O2 in expired air = 18 % of 100 l = 18 lVolume of O

2 used in 10 min = (21–18) l = 3 l

Volume of O2 used per min = 3/10 l = 0.3 l


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It is known that approximately 20 kJ of energy is released when 1 litre ofoxygen is consumed, so in the above example, EE would be:

EE = 20 × 0.3 = 6 kJ/min

The bag method is unsuitable for measuring the EE during physicalactivity.

Portable respirometers allow energy expenditure during numerousoccupational and sporting activities to be measured.

A respirometer measures the total volume of expired air passingthrough it and collects a small gas sample for subsequent analysis ofoxygen and carbon dioxide.

Measurements made using these respirometers form the basis ofpublished tables of the energy cost values of many activities.

Figures 19 and 20 illustrate the measurement of various activities usingthese portable respirometers.

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


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Figure 20: Measuring energy expenditure using a modern, lightweightportable respirometer.

In order to calculate the total energy expenditure of an individual, it isnecessary to have an accurately timed record of all the activities of theday in addition to the energy cost of each activity.

An activity diary, covering all 1,440 minutes of the day, should ideallybe kept for four to seven days in order to represent a typical pattern ofnormal life for the individual.

The energy cost of each activity can either be measured by indirectcalorimetry, as previously described, or estimated from publishedvalues.

Figure 21 shows a page from a typical activity diary, and Table 9 showshow total energy expenditure can be calculated for an individual.


BIOLOGY4 0

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

Table 9

Activity Duration Energy cost Total(min) (kJ/min) (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 10,370 kJ(10.4 MJ)


a.m. 0 1 2 3 4 5 6 7 8 9

9.00

9.10

9.20

9.30

9.40

9.50

10.00

10.10

10.20

10.30

10.40

10.50

Each page must add up to 120 min

S = 7 + 27 = 34STA = 15 + 30 = 45W

S= 23 = 23

WF

= 18 = 18Total 120 min

N.B. Only record when there is achange in activity

S

STA

WS

S

WF

STA

S = Sitting WS = Walking slowly

STA = Standing activity WF = Walking fast

BIOLOGY 4 1

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 oxygenconsumption during any activity above resting – the greater the oxygenconsumption, the higher the heart rate. This relationship between HRand EE will vary according to the fitness of the individual and willdepend on the type of activity being undertaken.

Figure 22 shows a plot of HR against oxygen consumption for twoindividuals of differing physical fitness. Subject A is able to work at aparticular intensity at a lower HR than the less fit Subject B.

Figure 22: The linear relationship between heart rate and oxygenconsumption in two individuals.

If the relationship between HR and EE is known for an individual, it ispossible to record HR over a 24-hour period using a ‘Sports Tester’.This is a lightweight transmitter applied to the chest by a belt withelectrodes on the inner surface. A watch-like device attached to the wristrecords HR continuously for up to 24 hours (or longer). The data canthen be downloaded to a computer for analysis to estimate energyexpenditure from the recorded heart rates.


BIOLOGY4 2

2.2 Body composition and weight control

Body composition is possibly the best indicator of the cumulative effectsof physical activity and nutrition. Low levels of aerobic activity andenergy-dense diets are likely to be the main reasons for the escalatingprevalence of obesity (excess body fat) in the developed world.

Body weight itself does not distinguish between excess weight (which isundesirable fat) and desirable muscle. In fact most successful weightmanagement programmes result from losing fat while maintaining oreven gaining lean tissue (muscle). This may often result in little changeor even an increase in body weight.

The most commonly used index of over- or underweight is called theBody Mass Index (BMI), calculated by dividing body weight (kg) byheight squared (m2).

Table 10 shows the currently accepted classification of overweight usingBMI, 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 25.0 – 29.9 IncreasedObese class I 30.0 – 34.9 Moderately increasedObese class II 35.0 – 39.9 Severely increasedObese class III Greater than 40 Very severely increased

Classification by BMI may result in an individual being classified asoverweight or obese, when in fact they have a relatively low % body fatbut a large muscle bulk.

Examples of such individuals are body-builders, weight-lifters and otherathletes with a well-developed musculature. For example, a body-builder 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.


BIOLOGY 4 3

Similarly, two individuals of the same weight and height may have BMIsin the ‘average’ range, but may have quite different % body fat.

In summary then, the many reasons for assessing body compositioninclude:

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

2. To monitor weight loss in an obese individual.

3. To monitor changes in body composition associated with certaindiseases (e.g. some cancers).

4. To monitor the effectiveness of exercise training programmes inathletes.

Measurement of body composition

For most purposes, the evaluation of body composition assumes that thebody 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 varyin complexity and accuracy.

There are a number of highly accurate laboratory methods which arecostly, time-consuming and are therefore restricted to relatively smallnumbers in a research setting.

Densitometry

For over thirty years, the most accurate method of assessing bodycomposition has been the measurement of body density by underwaterweighing.

This assumes that the fat mass and fat-free mass have fixed and constantdensities of 0.9 g cm–3 and 1.1 g cm–3 respectively, thereforemeasurement of an individual’s body density can predict the relativeproportions 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 bodymass (kg) measured in air dividedby body volume (l) which can bemeasured by weighing theindividual immersed in a tank ofwater. The difference between theweight in air and the underwaterweight is equal to the body volume(Archimedes’ Principle). Figure 24shows this technique beingperformed.

Figure 24: Measuring body densityby underwater weighing.


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Having calculated body density, % body fat is computed using amathematical 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 toAchimedes’ Principle, the weight loss in water of 58 kg is equal to theweight 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 cm3

= 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 watermay be difficult and produce anxiety in some individuals (e.g. children,the elderly).

A new method of measuring body density has been developed whichmay eventually replace underwater weighing. Instead of using water tomeasure body volume, the ‘Bod Pod’ uses air displacement. For thisprocedure, the subject sits inside a small chamber (the ‘bod pod’), andbody volume is computed by measuring the initial volume of the emptychamber minus the volume with the person inside (see Figure 25).


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Figure 25: The ‘bod pod’ thatmeasures body density through airdisplacement.

The advantages of this method overunderwater weighing are:

• short measurement time (5–8minutes)

• 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 compositionand involves measuring the layer of fat under the skin (subcutaneouslayer) at specific sites with a skinfold caliper (see Figure 26).

Figure 26: Measuring skinfold thicknesses with calipers.


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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. over the biceps muscle at the front of the arm2. over the triceps muscle at the back of the arm3. under the shoulder blade at the back (subscapular)4. 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 topredict 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 asmall 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 theapplied electric current can give an estimate of the lean / fat ratio in thebody – the higher the impedance value, the higher the % body fat.

Figure 28 shows the positioning of the individual for measurementusing BIA.

Figure 28: The position of body and electrode placement usingbioelectrical 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 oroedema) will affect the accuracy of the result

• tends to over-estimate body fat in very lean, muscular people andunder-estimate % fat in obese people.

Waist/hip ratio

It is now known that the distribution of fat in the body rather than thetotal 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 hipsand thighs).

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


BIOLOGY5 0

A simple way of estimating the fat distribution of individuals is tomeasure the ratio of waist circumference to hip circumference. Thosewith ‘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 0.8for women.

Weight control and obesity

A definition of obesity is ‘A chronic disease characterised by excessivelyhigh 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% ofwomen in 1980 to 17% of men and 20% of women in 1997. If this trendcontinues, it is predicted that the prevalence of obesity in the year 2010will be about 19% of men and 25% of women (see Figure 30).

Figure 30: The increasing rate of obesity since 1980.

The prevalence of obesity in Scotland is similar to that in England, with14% of men and 17% of women classified as obese (BMI > 30). Evenmore worryingly, about 20% of Scottish children are overweight.


% BMI >30

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BIOLOGY 5 1

Health risks of obesity

There are many health problems associated with obesity, including anincreased 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 mayall be involved. However, the two most likely causes of the steep rise inthe 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 thistime 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 energyexpenditure or a combination of both.

Current evidence would suggest that weight loss is more likely to bemaintained if levels of physical activity are increased by permanentlifestyle 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 adesirable level of body composition (12–15% fat in males, 20–30% infemales).

For individuals who are trying to lose weight by only reducing their foodintake, the addition of exercise has many benefits:

• increased energy deficit• increased relative loss of fat while preserving ‘active’ lean tissue


BIOLOGY5 2

• 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 1kgof body fat, regardless of whether this deficit occurs slowly or rapidly.For example, a deficit of 420 kJ /day between energy intake and energyexpenditure 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 fatloss after only fourteen days (2,100 × 14 = 29,400 kJ).

The effectiveness of exercise in weight-control programmes will dependon the target amount of body fat to be lost.

Example:

Let us assume that an individual wants to lose 10kg of body fat – thisrepresents a total energy deficit of approximately 294 MJ.

If the desired energy deficit is 2 MJ/day (which can be achieved byincreasing energy output by 1 MJ/day and reducing energy intake by1 MJ/day), then it would take approximately 147 days (21 weeks) to lose10kg of fat.

The same fat loss could be achieved by creating an energy deficit of only1 MJ/day, but this would take nearly a year to achieve.

Conversely, if the energy deficit was increased to 4 MJ/day, 10kg of bodyfat should be lost after only ten weeks (294 / 4 = 74 days = approx. tenweeks).

Many nutritionists recommend a fat loss of no more than 0.5–1.0kg perweek, which is achieved by an energy deficit of approximately 2–4MJ/day.

Aerobic forms of exercise of moderate intensity and reasonably longduration – e.g. brisk walking, jogging, swimming, cycling, golf, dancing –seem to be the most effective for fat loss in addition to conferring manyother health benefits.

Many health authorities, including the Health Education Board forScotland (HEBS), now recommend the accumulation of at least thirtyminutes of moderate-intensity physical activity over most days of theweek.


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2.3 Diabetes mellitus

This section examines the role of exercise in the treatment andprevention of diabetes mellitus, a disorder occurring in adults andchildren which results in a failure to control blood glucose levels and animpaired ability to store glucose in the form of liver and muscleglycogen.

Diabetics have additional health complications such as an increased riskof 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 andthen consider the pathophysiology of the disorder.

Control of blood glucose levels

Blood glucose levels must be kept between fairly narrow limits, and thisis normally achieved by storing excess glucose after a meal in the form ofglycogen in the liver and skeletal muscles. This prevents blood glucoselevels from becoming too high (hyperglycaemia).

The brain requires a constant supply of glucose, so between meals andafter an overnight fast, blood glucose levels are maintained by the liverreleasing glucose back into the bloodstream, thereby preventing bloodglucose from falling too low (hypoglycaemia).

Blood glucose levels are controlled mainly by the hormones insulin andglucagon, which are secreted by small clusters of cells scatteredthroughout the pancreas and known as the Islets of Langerhans. Beta(β) cells secrete insulin and Alpha (α) cells secrete glucagon.

The control of blood glucose levels by the opposing actions of insulinand glucagon is illustrated in Figure 31.


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Figure 31: The control of blood glucose levels through the actions ofinsulin and glucagon.

The secretion of insulin and glucagon is directly controlled by the levelof blood glucose that passes through the pancreas. An increase in bloodglucose (e.g. after a meal) stimulates insulin secretion and decreasesglucagon secretion. A reduction in blood glucose (between meals) leadsto a decreased insulin secretion and increased glucagon secretion.

This homeostatic control mechanism is an example of negative feedbackcontrol – increased blood glucose stimulates insulin secretion; insulinthen induces glucose entry into cells, which lowers the blood glucoseand reduces the stimulus to the pancreas for insulin secretion.

Insulin affects a number of different cell types, the principal targetsbeing skeletal muscle cells, liver cells and fat cells.


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Skeletal muscle cells and fat cells have a very low permeability to glucosein the absence of insulin. Insulin acts by stimulating the uptake ofglucose into muscle and fat cells.

By contrast, the cell membrane of liver cells is quite permeable toglucose, so glucose enters whether or not insulin is present. However,insulin still increases the uptake of glucose by liver cells and increasesglycogen formation.

Insulin is a protein hormone which binds to specific receptors in the cellmembrane of its target cells. These insulin receptor complexes result ina 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 insulinreceptors 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 amountsof 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 inonset and progress and is caused by the destruction of the insulin-producing β cells of the pancreas, which results in inadequate insulinproduction.

This commonly occurs in childhood and was previously referred to asearly-onset or juvenile-onset diabetes.

The treatment for Type 1 diabetes is regular injections of insulin, givensubcutaneously. Insulin cannot be taken orally because it is a proteinand would be digested by the gastro-intestinal enzymes.

Symptoms normally include fatigue, weight loss and weakness. Weightloss is caused by the body breaking down fat stores (and protein) tosupply 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 developslater in life (after age 40) and was previously known as adult-onset ormaturity-onset diabetes. It affects 3–7% of the adult population, andworldwide accounts for hundreds of thousands of deaths annually dueto an increased incidence of cardiovascular disease. It causes disabilityin millions.

It occurs mainly in overweight individuals – more than 80% of Type 2diabetics are or have been overweight.

In this condition, individuals can produce insulin, and have insulinlevels in the blood which are normal or higher than normal, but thetissues (especially the liver and skeletal muscles) become less sensitiveto it. This is known as insulin resistance. The target cells for insulinappear to have a deficiency of insulin receptors and this reduces theability of the skeletal muscle cells and fat cells to take up glucose.


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Most individuals develop insulin resistance before they develop thedisease, often as a consequence of becoming obese – i.e. they produceinsulin, but it cannot be used effectively by the cells. The pancreas triesto compensate for this resistance by producing more insulin. Eventuallythe β cells become ‘worn-out’ and insulin production decreases. Thisresults in an increase in blood glucose and diabetes develops.

In both types of diabetes, the inability to store glucose after a meal andthe limited uptake of glucose into the cells results in a rapid rise inblood glucose levels (hyperglycaemia). At very high levels, the kidneysare unable to absorb all the glucose passing through them and theexcess glucose appears in the urine. Glycosuria is often the first stage inthe diagnosis of the condition, from urine tests carried out as part of aroutine examination.

The excess glucose excreted in the urine carries with it a large volumeof 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 andis based on the fasting individual’s response to drinking a prescribedamount of glucose (50–100g) dissolved in 1 litre of water. Blood glucoselevels are then measured every thirty minutes over a two-hour period.

Figure 33 illustrates the results of a glucose tolerance test for a non-diabetic and a diabetic individual.


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Figure 33: Examples of glucose tolerance results for diabetic and non-diabetic subjects.

In the non-diabetic individual, blood glucose reaches a peak of7mmol l–1 thirty minutes after ingestion of glucose load, and falls to4mmol l–1 after two hours. This indicates that the pancreas has secretedadequate insulin to allow uptake of the additional glucose by the tissues.

In the diabetic individual (with either type of diabetes mellitus), fastingblood glucose level tends to be higher than normal and levels may riseabove 11mmol l–1 within thirty minutes of ingesting the glucose drinkand remain high for several hours.

Effect of exercise in prevention and treatment of non-insulindependent 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 inrelatively unfit individuals. It is also thought that a decrease in insulinsensitivity with advancing age can be prevented by regular exercise.


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The mechanism for this exercise-induced reduced insulin resistance isthought to be related to adaptations in skeletal muscle, includingincreased capillary network and blood flow. Enhanced glucose transportdue to an increase in the number of insulin receptors on the muscle cellmembrane, and increases in the enzymes associated with glucosestorage, are also thought to be related to exercise.

Improved insulin sensitivity (i.e. reduced insulin resistance) throughexercise training starts to be lost within five to seven days of the lastbout of exercise, emphasising the importance of regular frequentexercise. General recommendations are the same as for general health –moderate intensity exercise five to seven times a week to be built intothe lifestyle.

Many epidemiological studies (which look at the occurrence of diseasesin large populations) have shown an increase in the incidence of Type 2diabetes in parts of the world where it was previously uncommon.

Heredity cannot account for this large increase over a relatively shorttime span, and it is more likely to be due to changes in lifestyle –decreased physical activity accompanied by high-energy diets whichleads to obesity, a major risk factor for Type 2 diabetes.

The relationship between obesity and Type 2 diabetes can be clearlyseen in Japanese Sumo wrestlers who are massively obese and mustconstantly over-eat to maintain their size. The incidence of Type 2diabetes amongst these wrestlers is reported to be 60% compared with5% in the general Japanese population.

Regular aerobic exercise can play an important role in preventing and/orcontrolling Type 2 diabetes by reducing body weight, or moreimportantly, body fat, which in itself reduces many of the risk factors forthe Type 2 diabetic. Obese individuals are more at risk of developingType 2 diabetes and it is believed that 80–90% of overweight Type 2diabetics can normally achieve metabolic control by following a low-energy 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 becomeprogressively more porous and brittle, increasing the risk of fractures.The bones become so weak that fractures can occur after only a minorfall, such as when stepping off a kerb. The wrist, spine and hip are thecommonest 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 re-assemble. In such cases, treatment is by surgical replacement of theaffected joint with an artificial joint.

Other effects of osteoporosis include loss of height, curvature of thespine 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 tosome extent, while 75% of those over 90 are affected. Men and childrenmay 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 lateadolescence, bones stop growing in length but become increasinglydense. In healthy, physically active individuals with an adequate calciumintake in the diet, peak bone density is reached in the late twenties andearly thirties.

Thereafter, in females, bone density starts to decline at the rate of about1% per year, resulting in loss of bone tissue and strength. After themenopause 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 of50, when density decreases at the rate of 0.4% per annum and does notusually cause significant problems until men are in their eighties.

Children who consume extra calcium and Vitamin D in the growingyears lay down more calcium in their bones than children on lessadequate intakes. Ninety-nine percent of the body’s calcium is containedin the skeleton, and when the diet is low in calcium, the body draws onits calcium reserves in the bone to make up the deficit. Therefore, whenpeople reach middle age, those who formed dense bones during theirchildhood and teens are at an advantage.

Hormones and bone growth

Between puberty and the menopause, oestrogen maintains bone tissueby stimulating the formation of new bone.

The lower levels of oestrogen produced by the post-menopausal womanreduce the activity of bone cells, thereby increasing the risk of calciumloss from the bones. Oestrogen is thought to enhance intestinal calciumabsorption and limit its withdrawal from bone, although the exactmechanism of this protective effect is unclear.

Men are at relatively low risk of developing osteoporosis as they havelarger, 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 massthan their less active counterparts of the same age. It appears thatregular exercise may help to slow the rate of skeletal ageing, regardlessof 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-riddenfor any length of time. Astronauts in zero gravity also experience loss ofbone density.

Bone becomes stronger as a result of the mechanical stress placed on itby the pull of the skeletal muscles in weight bearing exercise. Walking,dancing, jogging, etc. are all thought to increase bone density, whilenon-weight bearing activities such as swimming are thought to have littleeffect on bone density.

Additional benefits of such exercise include the strengthening oftendons, ligaments and their points of attachments to bones.

Therefore, weight bearing exercise should be regarded as essential forthe development and maintenance of healthy bones, particularly forwomen in their twenties and thirties who must maximise bone densitybefore age-related losses occur later in life.

Resistance exercise also strengthens bones. This involves moving objectsor the body weight to create a resistance – e.g. weight training. Studiesof tennis players show a higher bone density in their racquet armsbecause these encounter much more resistance. In addition tostrengthening bones, this type of exercise also helps co-ordination andbalance, 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 inconjunction with other treatments such as hormone (oestrogen)replacement therapy (HRT) or calcium supplements to halt or evenreverse the progress of the disease.

For example, forty-five minutes of moderate exercise three times a weeknot only reduces the rate of calcium loss in older individuals but alsostimulates calcium deposition in the bones.

However, exercise programmes for individuals with osteoporosis mustbe carefully designed to avoid the risk of osteoporotic fractures. Walkingand activities of moderate intensity can prevent further calcium losswithout increasing the risk of fractures.

The risks of exercise in female athletes

Although exercise is known to be beneficial for bone health, extremelevels of exercise undertaken by some young female athletes mayactually cause osteoporosis.

When female athletes undergo very intensive training, often combinedwith a restricted diet, they may reduce their body fat to such a level thatthe menstrual cycle ceases. This results in reduced levels of oestrogenand loss of its protective effects on bone, making the women moresusceptible to calcium loss and reduced bone density. This is particularlyserious when it occurs during a period of potential growth, e.g.adolescence. Some studies have found that bone density in some youngfemale athletes is similar to that found in women in their seventies.Unfortunately, these bone losses are thought to be irreversible. Thiscombination of intensive training, restricted diet and low body fat issometimes referred to as the ‘female athlete’s triad’.

Treatment of osteoporosis

In summary, osteoporosis is a very common bone disease affecting manypeople (particularly women) from middle age onwards.

Prevention of osteoporosis is far better than any treatment as the age-related loss of bone mass is not so devastating if the bone mass is welldeveloped before the disease sets in. Weight bearing exercise takenregularly increases the bone mass. This, combined with an adequate


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dietary intake of calcium and vitamin D, are all important in theprevention of osteoporosis.

For post-menopausal women, hormone replacement therapy to replacethe decreased oestrogen production is often recommended.


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The bibliography contains full references for all sources used in thepreparation of this monograph.

Bird S R, Smith A and James K (1998), Exercise Benefits andPrescription, Stanley Thornes (Publishers) Ltd, ISBN 0-7487-3315-9.Chapter 11 of this text provides an excellent review of the currentliterature 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 0-397-51091-8

Dept of Health (1991), Dietary Reference Values for Food Energy andNutrients for the United Kingdom. Report on Health and Social Subjectsno. 41. London, HMSO, ISBN 0-11-32197-2

McArdle W D, Katch F I and Katch V L (1994), Essentials of ExercisePhysiology, Lea and Febiger, ISBN 0-8121-1724-7. This text is highlyrecommended as additional background reading for this unit. The moreadvanced texts by the same authors (listed below) are also excellent butsomewhat more complex.

McArdle W D, Katch F I and Katch V L (1999), Essentials of ExercisePhysiology (2nd Edition), Lippincott, Williams and Wilkins, ISBN 0-683-30507-7 (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 andFebiger, ISBN 0-8121-1351-9

McArdle W D, Katch F I and Katch V L (1999), Sports and exercisenutrition, Lippincott, Williams and Wilkins, ISBN 0-683-30449-6

McKenna B R and Callander R (1990), Illustrated Physiology (5thEdition), Churchill Livingstone, Edinburgh, ISBN 0-443-04095-8

BIBLIOGRAPHY

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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 HumanAnatomy and Physiology, West Publishing Co, ISBN 0-314-00602-8

Torrance, James (1995), Higher Grade Human Biology, Hodder andStoughton, ISBN 0-340-63908-3

Tortora G J and Grabowski S R (1993), Principles of Anatomy andPhysiology (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), UnderstandingNormal and Clinical Nutrition (4th Edition), West Publishing Co, ISBN0-314-04178-8

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/

BIBLIOGRAPHY

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Adenosine triphosphate (ATP) Compound having a nitrogen base,ribose and three phosphate groups; known as the ‘energy currency’ ofthe cell.

Adrenaline Hormone secreted by the adrenal medulla in times of stress.

Angina pectoris Pain in the chest usually resulting from an inadequateblood 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 whichdevelops in the arterial walls in atherosclerosis. Also known as plaque.

Atherosclerosis A disease of the arteries in which lipid-containingsubstances are deposited on the arterial walls, causing a narrowing oftheir diameters.

Atrioventricular (AV) valves Heart valves located between the atria andthe 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 energyin the resting, fasted state.

Bioelectrical impedance analysis (BIA) A method of estimating bodyfat by measuring the resistance of the body to the flow of a low-intensityelectric current.

Blood pressure (BP) The force exerted by the blood against the walls ofblood vessels.

Body composition The division of the body into fat and fat-freecomponents.

Body mass index (BMI) The ratio of body weight to height squared;used as a crude measure of obesity.

GLOSSARY

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Bomb calorimeter An instrument that measures the heat energyreleased when foods are burned, thereby providing an estimate of theenergy value of the food.

Capillaries The smallest type of blood vessels; they connect arterioleswith venules and have thin walls only one cell thick to allow substancesto enter and leave the blood.

Cardiac cycle One complete heart beat, including atrial contraction andrelaxation, ventricular contraction and relaxation and the short periodwhen the entire heart is relaxed.

Cardiac output (CO) The volume of blood ejected from each ventricleper minute.

Cardiovascular disease (CVD) A general term for all the diseases of theheart and blood vessels, including coronary heart disease,atherosclerosis, angina pectoris and stroke.

Cardiovascular system (CVS) Body system consisting of the heart andblood vessels.

Cerebrovascular accident (CVA) See stroke.

Cholesterol A type of lipid that is a component of cell membranes and isused 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 associatedblood vessels supplying the heart.

Densitometry A body composition method used to estimate bodyvolume by measuring weight loss when the body is totally submergedunder water (underwater weighing).

Diabetes mellitus A disease characterised by an abnormally high levelof glucose in the blood usually caused by insufficient (Type 1) orrelatively inefficient (Type 2) insulin secretion.

Diastole Relaxation of a heart chamber; usually refers to relaxation ofthe ventricles.

Diastolic blood pressure (DBP) The lowest pressure exerted by theblood against the arterial walls during relaxation of the ventricles.

GLOSSARY

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Direct calorimetry The measurement of energy expenditure from theheat energy emitted from a body.

Echocardiography The use of ultrasound to examine the valves andchambers of the heart.

Embolism A blood clot that breaks loose from accumulated matter inthe blood vessels and travels through the circulatory system.

Energy balance The state when energy intake is equal to energy outputand body fat stores are constant.

Fat-free mass (FFM) All fat-free chemicals and tissues in the bodyincluding 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 thatincreases blood glucose.

Glucose tolerance test A blood test used for the diagnosis of diabetesmellitus; measures the blood glucose levels over several hours inresponse 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 transportscholesterol back to the liver from the peripheral cells; known as ‘goodcholesterol’.

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 ofdiabetes occurring mainly in young people, caused by lack of insulinbrought on by damage to insulin-producing cells in the pancreas. Alsoknown as Type 1 diabetes or early-onset diabetes.

GLOSSARY

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Indirect calorimetry Estimation of energy expenditure frommeasurement of the amount of oxygen used by the body.

Insulin A hormone secreted by endocrine cells in the pancreas whichdecreases blood glucose by increasing cellular uptake of glucose.

Insulin resistance Condition in which cells become less responsive toinsulin; they cannot take up as much glucose despite adequate insulinproduction.

Ischaemia Lack of oxygen (usually temporary) caused by a decreasedblood flow to a group of cells or tissues.

Islets of Langerhans Clusters of endocrine cells in the pancreas whichsecrete insulin (β cells) and glucagon (α cells).

Kilocalorie (kcal) Unit of energy defined as the amount of energyrequired 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 cellmembranes and for steroid hormone synthesis. Known as ‘badcholesterol’ as high blood levels of LDL are strongly linked withincreased risk of heart disease.

Myocardial infarction (MI) Damage to the heart muscle caused byblockage of the coronary arteries. Commonly referred to as a ‘heartattack’.

Negative feedback A type of control in which a stimulus (e.g increase inbody temperature) initiates actions which reverse that stimulus (i.e.reduce body temperature).

NIDDM Non-insulin dependent diabetes mellitus; commoner type ofdiabetes occurring mainly in individuals over 40, resulting from a loss oftissue responsiveness to insulin. Also known as Type 2 or late-onsetdiabetes.

Obesity A disease characterised by excessively high body fat in relationto lean body tissue.

GLOSSARY

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Osteoporosis A condition characterised by a reduction in bone densityleaving bones brittle and fragile; commonly seen in post-menopausalwomen and elderly men.

Peak bone density The highest attainable bone density for anindividual; developed during the first three decades of life.

Physical activity ratio (PAR) The energy cost of an activity expressedas a multiple of the BMR; e.g. PAR for ‘walking at average speed ‘ is2.8 × BMR.

Platelets Cell fragments found in blood that function in the clottingprocess.

Plaque See atheroma.

Pulmonary circuit Short circulatory loop carrying deoxygenated bloodfrom the right ventricle to the lungs and returning oxygenated bloodfrom the lungs to the left atrium.

Semi-lunar valves Valves which lie between the aorta and the leftventricle and between the pulmonary artery and the right ventricle.

Sphygmomanometer An instrument for measuring arterial bloodpressure.

Stroke Destruction of the brain tissue resulting from blockage of bloodvessels which supply the brain. Also known as a cerebrovascular accident(CVA).

Stroke volume (SV) The volume of blood ejected by a ventricle perbeat.

Systemic circuit System of blood vessels which carry oxygenated bloodfrom the left ventricle to all the organs of the body and returndeoxygenated blood to the right atrium.

Systole In the cardiac cycle, the phase of contraction of the atria orventricles.

Systolic blood pressure (SBP) The highest pressure exerted by bloodagainst the walls of the arteries during ventricular contraction; about120 mm Hg under resting conditions for a young healthy adult.

GLOSSARY

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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 clotresulting in a myocardial infarction or heart attack.

Thrombus A blood clot which may obstruct a blood vessel or the heartcavity.

Total peripheral resistance (TPR) The sum of all resistances of allsystemic blood vessels.

Type 1 diabetes See IDDM.

Type 2 diabetes See NIDDM.

Vasoconstriction A narrowing of a blood vessel caused by contractionof the smooth muscle lining the vessel.

Vasodilation The widening of a blood vessel caused by relaxation of thesmooth muscle lining the vessel.

Veins Blood vessels which carry blood from the tissues back to theheart.

Ventricles The two larger, lower heart chambers.

Venules Small veins that collect blood from capillaries and deliver it toveins.

VO2max

A measure of the maximum amount of oxygen that a person canutilise; used as a measure of aerobic fitness.

GLOSSARY

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Physiology helath and Exercise (Part 2)

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