Anaerobic processes of ATP generationDuring muscle contraction, ATP is the direct connecting link between fibre shortening (orlengthening), force development and metabolism. In this process, the ATP turnover in muscle ismost significantly determined by the quantity of calcium released from the transverse tubularsystem. The most important regulatory enzymes responsible for energy release from ATP areATPase like actomyosin-ATPase, Na+/K+-ATPase and sarcoplasmatic reticulum Ca2+-ATPasewhich, in turn, are activated by calcium. The maximum quantity of ATP that can be hydrolyzedduring a single contraction depends on the myosin isoenzyme pattern and, therefore, on the type ofmuscle fibre. In addition, muscles contain phosphocreatine (PCr), which is another high-energyphosphate compound and stored in muscle tissue at a concentration three times that of ATP.Because of the small quantity of ATP available in the cell, the breakdown to ADP immediatelystimulates the breakdown of PCr to provide energy for ATP resynthesis. This reaction is catalyzedby the enzyme creatine kinase (CK):In other words, a fall in the ATP concentration is buffered by PCr, and therefore the ATPconcentration in the muscle remains nearly constant at a high level during physical exercise. Evenunder extreme physical strain leading to exhaustion, the ATP concentration rarely falls below 50%of the baseline value. The ‘high energy phosphate’ system, however, is limited by the fact that thequantity of releasable phosphate for the energy-production from the high-energy phosphates (PCrand ATP) during high intensive work is drastically reduced. During short-term intensive physicalexercise followed by longer phases of regeneration, or during low-intensity physical loads, high-energy phosphates are mainly re-phosphorylated by the oxidative pathway. The capacity forresynthesis depends on the oxidative capacity of the respective system. In contrast, at highlyintensive physical loads of longer duration, the PCr concentration drops rapidly and drastically. Inthis case, the resynthesis occurs through the anaerobic energy provision from carbohydrates, whichleads to the production of lactic acid, a process named anaerobic glycolysis, because this processdoes not require oxygen.Glycolysis from glycogen:An increase in pyruvate, NADH/NAD+ ratio or H+ are metabolic changes that will promote lactateformation. Oxygen deficiency, increased recruitment of fast twitch fibers and low aerobicconditions in the exercising muscle are conditions for this metabolic imbalance. NADH + H+ can bere-oxidized only by the reduction of pyruvate, catalyzed by lactate dehydrogenase (LDH). Lacticacid is produced in this process. The process of NADH - H+ re-oxidation through pyruvate is a veryuneconomical interference because only three moles of ATP are obtained from the degradation permole glycosyl unit, whereas 36 moles/38 moles of ATP can be formed during complete oxidation.Glycogen phosphorylase plays a key role in anaerobic glycolysis. It breaks down the muscleglycogen and is regulated by Ca2+ released from the transverse tubular system through the enzymephosphorylase-kinase. Generally, the reduced Ca2+ release from the tubular system duringcumulative fatigue is an indication of the importance of Ca2+ in muscle fatigue. Also the enzymephosphofructokinase, which catalyzes the transformation of fructose 6-phosphate to fructose 1.6-diphosphate in the cytoplasm of the muscle cell, appears to play a decisive role in anaerobicglycolysis in the sense that it is inhibited by the sinking pH value due to the lactic acid productionand thus limiting the anaerobic glycolysis. In fact, H+ ion concentrations influence glycolysis andthe PCr concentration during physical exercise.   A high H+ concentration reduces the PCr levelthrough the enzyme creatine kinase. Furthermore, local acidosis in the working muscles appears to
further reduce the formation of cross-bridges between the myosin heads and the actin molecules ofmuscle fibers. In this context, it should be mentioned that a metabolic acidosis is not an absoluteprerequisite for muscle fatigue because patients with a congenital glycogen phosphorylasedeficiency (McArdles disease) are prone to early fatigue despite the fact that they have no lactateacidosis.During high intensive exercise, lactic acid can be accumulated for two reasons. As a result of theextremely high glycolysis rate which occurs under intensive physical strain, pyruvate is formed insuch large quantities that it cannot be utilized by the mitochondria. In addition, the reduced NADH+ H+ occurring in the cytoplasm of muscle cells during glycolysis cannot be re-oxidized at asufficient rate by the mitochondrial membrane. When very intensive exercise continues to persist,which requires continued anaerobic energy production, the buffer capacity of the organism isexceeded and lactic acid accumulates. Based on these theoretical considerations, the concentrationof lactic acid in muscle and blood serves as a reference point for the interaction of the aerobic–anaerobic metabolism under physical strain. Therefore, lactate can be used as one of the mostimportant parameters to determine endurance performance and also to optimize the trainingprocesses ( Fig. 2.1 ).Figure 2.1 Model of the lactate performance curve and the energy supply during increasing work load.This can be recognized by plotting the blood lactate concentrations versus VO2 (l × min-1; ml × kg ×min-1) during an exercise test with increasing work loads. During the first minutes or even first loadsteps, the blood lactate concentration as an indirect measure of the lactic acid produced in theexercising muscles remains stable because the energy demand, meaning the ATP-resynthesis rate ismet by oxidation of fats and carbohydrates. Although at the beginning of the exercise or whenincreasing the workload step by step, lactate will be produced in the working muscles because ofthe delay of the cardio-respiratory supplying reactions, lactate will be metabolized within themuscles and will not be carried to other compartments like blood, a process which is called ‘cell tocell shuttle’. From a certain point, when the exercise intensity is higher, fast twitch muscle fiberswhich have a lower oxidative potential and therefore produce more lactate have to be activated and
therefore lactate in the exercising muscles is formed and the blood lactate concentration willincrease. This point, which is called the aerobic threshold or first lactate turn point is the beginningof a so-called ‘mixed aerobic-anaerobic metabolism’. With increasing intensity a second deflectionpoint can be observed, when more lactate in the exercising muscle will be produced than can bebuffered or even removed. From this point called the anaerobic threshold or respiratorycompensation threshold, or the second lactate turn point, lactate production increases rapidly, willbe accumulated and finally leads to the end of the exercise. If one contrasts the so called ‘lactate-performance-curve’ of an untrained person, a marathon runner and a 400-m runner, the differencesin the interaction of the aerobic–anaerobic metabolism can easily be seen. The untrained personshows a very rapid increase and accumulation of the blood lactate concentration from the restingvalue. In contrast, in the endurance-trained marathon runner, the lactate level remains low withincreasing workloads, which is the result of the aerobic adaptations by the endurance training. Thatmeans that both – the first and the second lactate turn points – occur at a higher percentage of theathletes maximal aerobic power. On the other hand, the production rate of lactic acid and resistanceagainst lactate accumulation is decreased. In contrast, the 400-m runner shows an earlier increase ofthe lactate production because of the specific metabolic adaptations resulting from anaerobictraining. Furthermore, the increase of the blood lactate concentration over the anaerobic threshold(second lactate turn point) is longer and more flat, showing that the muscle cells can tolerate theacidification resulting from increasing lactate accumulation better as a consequence of the anaerobictraining ( Fig. 2.2 ).Figure 2.2 Lactate-performance curves and heart rate performance curves of three different trained individuals.Aerobic processes of ATP generationIn contrast to the anaerobic energy system which provides energy at a high liberation rate but withlimited supply, muscles need a continuous supply of energy at rest and during long duration but lowintensive activities. This is provided by the oxidative (aerobic) system which has a lower energy
liberation rate but a tremendous energy yielding capacity. Aerobic production of ATP occurs in themitochondria and involves the interaction of the citric acid cycle (Krebs Cycle) and the electrontransport chain. Oxygen serves as the final hydrogen acceptor at the end of the electron transportchain. The term maximal aerobic power (VO2max, VO2peak) reflects the amount of ATP which canbe produced aerobically and therefore the rate at which oxygen can be transported by thecardiorespiratory system to the active muscles. From resting metabolism (3.5 ml/kg per min) theaerobic power production can be increased up to peak values of 35–38 ml/kg per min and 42–45ml/kg per min in untrained women and men, respectively. Values of 72–76 ml/kg per min and 85–90 ml/kg per min have been reported in endurance-trained female and male athletes, respectively.Oxidation of carbohydrateThe first step in the oxidation of carbohydrates is the anaerobic breakdown of muscle glycogen andblood glucose to pyruvate. In the presence of oxygen, pyruvate – the end product of glycolysis – isconverted into acetyl-coenzyme A (acetyl-CoA), which enters the Krebs Cycle (citric-acid cycle).The Krebs Cycle is a complex series of chemical reactions that breaks down these substrates intocarbon dioxide and hydrogen and forming two ATPs. In addition, six molecules of reducednicotinamide-adenine-dinucleotide (NADH) and two molecules of reduced flavin-adenine-dinucleotide (FADH 2) are also produced from the glucose molecule, which carry the hydrogenatoms into the electron transport chain where they are used to re-phosphorylate ADP to ATP(oxidative phosphorylation). The complete oxidation of one glucose molecule in skeletal muscleresults in a net yield of about 36 or 38 ATPs depending on which shuttle system is used to transportNADH to the mitochondria ( Fig. 2.3 ).
Figure 2.3 ‘Flow sheet’ for energy yielding processes from lipids, carbohydrates and proteins. (Redrawn from Smekal 2004.)Oxidation of fatFat can only be metabolized in the presence of oxygen. The triglycerides are stored in fat cells andwithin the skeletal muscles and serve as a major energy source for fat oxidation. For this to happen,the triglycerides are broken down by lipases to their basic units of one molecule of glycerol andthree molecules of free fatty acids (lipolysis). After having entered the mitochondria, the free fattyacids undergo a series of reactions in which they are converted to acetyl-coenzyme A, a processcalled beta-oxidation. From this point, the fat metabolism then follows the same pathway as thecarbohydrate metabolism when acetyl coenzyme A enters the Krebs Cycle and the electrontransport chain. While the ATP-amount produced varies depending on the oxidation of differentfatty acids, the complete oxidation of one (18-carbon) triglyceride molecule results in a total energyyield of about 460 ATPs. Although triglyceride oxidation provides more energy production pergram than carbohydrates, the oxidation of fat requires more oxygen, meaning that fat mostly isoxidized at rest or during moderate exercise when oxygen delivery is not limited by the oxygentransport system. At rest, e.g. the ratio of ATP-production is up to 70% of fat and 30% fromcarbohydrates, whereas during high intensity exercise, the majority of energy or even the totalenergy comes from carbohydrates.
Oxidation of proteinsOxidation of proteins is also utilized to obtain energy at rest as well as during physical exercise.Several amino acids (especially leucine, isoleucine, alanine and valine) contribute to the productionof energy. The access to amino acids increases in proportion to the load intensity of any physicalactivity, but the proportion of energy provided by amino acids during physical exercise appears tobe limited to about 10%. However, of practical significance is the fact that amino acids are oxidizedin greater quantities when the caloric supply is insufficient and also in the presence of acarbohydrate deficiency. This leads to catabolic states (degradation of functional proteins) and lossof nitrogen. The degradation of functional proteins is problematic because muscles are affected bythis phenomenon, which obviously has a detrimental effect on performance capacity.Power and capacity of energy yielding processesAn important approach to a better understanding of energy demand and energy supply duringphysical activity and sports is the question as to which substrates are utilized for the production ofenergy at specific intensities. An important factor in the selection of the substrate is the rate atwhich energy can be released from the respective substrate, i.e. the maximum achievable release ofenergy per time unit. Therefore, the maximal intensity of the exercise is limited by the (combined)maximal power of the energetic processes.The ‘high energy phosphates-system’ provides the highest rate of energy liberation, but its capacityis limited to only 3–7 s and therefore needs to be replenished constantly providing other processesfor ATP resynthesis on a lower energy liberation rate, the glycolytic (anaerobic) and the oxidativecombustion of fuels.The glycolytic pathway can provide energy rapidly because of the high concentration of glycolyticenzymes and the speed of the chemical reactions involved. However, glycolysis cannot supply asmuch energy per second as the ATP-PC system. At high intensity exercise, the highest energyliberation from glycolysis occurs during the first 10–15s because acidification of muscle fibersreduces the breakdown-rate of glucose and glycogen. This impairs glycolytic enzyme function anddecreases the fibers calcium binding capacity and thus muscle contraction. This causes an increaseof the muscle lactate up to more than 25–30 mmol/kg wt, and later one of blood lactate up to 18–25mmol/l ( Table 2.1 ).Table 2.1 -- Power and Capacity of Energy Yielding Processes in Human Muscle Power (mol ATP/min) Capacity (mol/ATP)Pcr 2.5 0.37Lactate 1.9 0.94CHOox 1.1 59FFAox 0.6 Not limitedPcr, phosphocreatine; CHOox, carbohydrate oxidation; FFAox, free fatty acid oxidation. Fordetails, see Henriksson and Sahlin 2002.The muscle cells capacity for anaerobic glycolysis during maximal physical activity is for a periodof approximately 1–3 min (shorter or longer depending on the intensity). Activities such as the 200-m free-style swim, 400-m sprint and strength-training activities with short rest periods between sets(e.g. 30 s) rely primarily on glycolysis for energy liberation. Anaerobic systems also contribute to
energy production at the beginning of less intense exercise, when oxygen uptake kinetics lag behindthe total energy demand placed on the system.Stored carbohydrates supply the body with a rapidly available form of energy with 1 g ofcarbohydrate yielding approximately 4.1 kcal (17.1 kJ) of energy. Under resting conditions, muscleand liver take up glucose and convert it into a storage form of carbohydrate, called glycogen, whichis, when needed as an energy source, broken down into glucose and can be metabolized to generateATP anaerobically and aerobically.The carbohydrate stores of the human organism are limited. They are composed of the circulatingglucose in blood, and carbohydrates which are stored in the form of glycogen in the muscle andliver. The quantity of carbohydrates which can be stored in the form of glycogen in the skeletalmuscles depends on a number of factors (e.g. nutrition, the state of training, muscle mass, thecomposition of muscle fibers and several other factors). Therefore, published data about thequantity of stored glycogen in the entire musculature vary between 1000 and 1900 kcal or evenslightly more in trained athletes after carbohydrate loading. Taking into consideration that themuscles needed for physical exercise (e.g. the marathon run or biking) only constitute a part of theentire muscle mass, the carbohydrate reserves of the working musculature must obviously beregarded as an important limiting factor during physical strain of long duration and/or highintensity. The liver also has a storage pool of about 60–80 to a maximum 120 g of glycogen,corresponding to an energy reserve of about 240 to a maximum of 490 kcal. It is important tomention that hepatic glycogen has another important function: it maintains the supply of bloodsugar to the brain, which is also important during exercise of high intensity or long duration ( Table2.2 ).Table 2.2 -- Body Stores for Fuels and Energy[a] Grams kcal Untrained Trained Untrained TrainedCarbohydrates Liver glycogen ∼80 ∼120 ∼328 ∼492 Muscle glycogen ∼250 ∼400 ∼1025 ∼1640 Glucose in body fluids ∼15 ∼18 ∼62 ∼74 Total ∼345 ∼538 ∼1415 ∼2206Fats Subcutaneous 8000 6000 74 000 55 880 Intramuscular 50 300 465 2790 Total 8050 6300 74 465 58 670Amino acids 100 110 410 451Proteins 6000 7000 – –a Estimates based on body size of 70 kg and 12% body fat (male).Carbohydrates are used preferentially as energy fuel at the beginning of exercise and during highintensive loads requiring more than 70% of the maximum oxygen uptake. Compared with theanaerobic energy breakdown, the rate of energy liberation with the oxidation of carbohydrates isabout one half and its capacity depends on the amount of glycogen stored in the muscles and in theliver. Without any substitution of carbohydrates during a long duration exercise, carbohydrate
capacity allows endurance exercise for about 60–90 (120) min depending on the involved muscularsystem and the intensity of the physical activity.Because muscle glycogen stores are limited and can become depleted during longer lasting vigorousexercise, an adequate diet especially for endurance exercise must contain a reasonable amount ofcarbohydrates, which enhance glycogen synthesis and also glycogen stores in muscles and liver.Fats are stored well in the organism but oxidized rather slowly. In order to utilize fat from fatdeposits as a source of energy, they must be mobilized and transported to the muscle cell in theblood in the form of free fatty acids, bound to albumin. However, fats are also present within themuscle in the form of fat cells between muscle cells, and in the form of droplets inside muscle cells.At low intensities, a large portion of the energy is provided by fat metabolism – mainly by the freefatty acids in plasma. If the intensity of physical activity is increased further, intramuscular fats andcarbohydrates are utilized in greater measure to fulfill the energy requirements. Fat oxidation doesnot increase at higher load intensities, but it is rather markedly reduced. A large body of data showsthat the limitation is particularly within the mitochondria. This is also evidenced by the fact that theoxidation of intramuscular fats seems to occur in an incomplete fashion. The most likely theory atthe present time points to a blockade of the transport of long-chain fatty acids through the innermitochondrial membrane when the rate of glycolysis is high (high intensity load). However, it isevident that in the presence of a markedly increased oxidative capacity of mitochondria, which isfound in persons who have undergone endurance training, larger quantities of metabolites resultingfrom beta-oxidation can be oxidized. In other words, at the same load intensity, less metabolites areformed during glycolysis – which, in turn, has a positive effect on fat oxidation ( Fig. 2.4 ).Figure 2.4 Total energy supply and relation of fat and carbohydrates during incremental workload. (Estimated from data by Achten andJeukendrup 2003.)As discussed earlier, even in persons with a very good endurance performance, the energy flow ratefrom fat is limited. If one assumes that the energy requirements for various sports increase with theload intensity, carbohydrates must be utilized to an increasing extent to provide the required energy,because energy flow rates from carbohydrates markedly exceed those that could possibly result
In the ancient Olympic Games, at the end of the third century BC, according to Galen and otherauthors of the time, athletes believed that drinking herbal teas and eating mushrooms could increasetheir performance during the competitions. Another interesting form of doping of this time was toprepare a powder with the oil, dust and sweat adhering to the skin of the athlete after thecompetition. This mix was removed in the dressing room with the ‘strigil’, a metallic instrumentwith the shape of an ‘L’ as show in Figure 4.1 . The athlete sold it to other participants, whobelieved that by drinking the mix, they would have the same physical capabilities of the champion,a myth that was not accepted by Judge Conrado Durantez, a Spanish historian of the AncientOlympia.Figure 4.1 Greek ancient athletes using the ‘strigil’ after a competition. (Source: Olympia Museum.)In the South-American sub-continent, stimulants ranging from harmless tea and coffee, up tostrychnine and cocaine, were used to increase performance. Spanish writers report a use from theIncas of chewing coca leaves, to help cover the distance between Cuzco and Quito, in Ecuador. In1886, the first fatality caused by doping was reported, when a cyclist named Linton died after anoverdose of stimulants in a race between Bordeaux and Paris.
role in oxygen transport. Inadequate iron intake, absorption or excessive loss limits the amount ofiron available for this and other intracellular processes.Iron deficiency anemia is common in non-athletic populations and is likely the most commonnutritional deficiency in the western world. The issue of whether iron deficiency is more common inathletes has always been a point of controversy. Large studies have shown that iron deficiencyoccurs in about 20% of menstruating women and 1–6% of postmenopausal women and men.Some studies have shown a higher prevalence of iron deficiency in female athletes than the generalpopulation, while others have failed to show a difference when compared with proper controls.  This suggests that exercise itself is not a risk factor for the condition, but athletes may be moreprone to developing it.Pseudoanemia, although not a true anemia, is the most common anemia in endurance athletes. Asmentioned in earlier, endurance athletes tend to have lower Hb levels than the general populationdespite a normal red cell mass. This is due to an expansion of plasma volume and a subsequentdilutional effect. This ‘sports anemia’ due to dilution of RBCs is referred to as pseudoanemia and isan adaptation of exercise and does not seem to inhibit athletic performance. It is not a pathologiccondition and it normalizes with training cessation in 3–5 days. The Hb level in a well-conditionedathlete may be 1–1.5 g/dl lower than the laboratory quoted ‘normal’. The physician looking afterathletes must be able to recognize this as a pseudoanemia and exclude iron deficiency anemia.There is no treatment for pseudoanemia other than recognizing it as distinct from other pathologicalanemias.Footstrike hemolysis refers to the bursting of RBCs in the circulation, from the impact offootfalls. Rowing and swimming also have been shown to have similar intravascular hemolysisand hence, such destruction of RBCs may be due to exertion as opposed to the footstrike itself.This hemolysis is usually mild and rarely if ever drains iron stores and causes anemia. Diagnosiscan be made when one has the combination of an elevated red cell volume, reticulocytosis and alow serum haptoglobin. Treatment revolves around lessening the foot impact, i.e. wearing well-cushioned shoes, attaining and maintaining an ideal weight and running on soft surfaces. It isunknown at this point how to treat hemolysis from non-impact sports, however, since it is so mild,treatment is rarely required.Relation to sportThe underlying development of iron deficiency anemia is either due to blood loss or poor ironintake through diet. Other sources have been suggested but do not appear to contribute to aclinically apparent anemia. Iron loss in sweat accounts for a very minimal amount. Similar studies(Fields 1997) have been done investigating iron loss from urine, the GI tract or from footstrikehemolysis; none of these appear to deplete iron stores in sufficient amounts to cause anemia. Themain culprit then seems to be dietary in nature. Athletes, especially women, involved in sports suchas long-distance running, ice skaters and gymnasts, through restrictive diets, consume too little ironto meet their daily needs. Vegetarian athletes are particularly at risk because the iron in vegetablesand grains is not as readily absorbed as that in red meat.Signs and symptomsAthletes with iron deficiency anemia may be asymptomatic, while others may experience muscleweakness, palpitations or shortness of breath. They usually seek medical attention because offatigue or decreased performance. A complete history should be taken to rule out significant GI orGU sources, although this is uncommon in a younger population, it may be significant in olderathletes.Investigations
Aging is associated with a progressive decline in most biological functions, but changes aresomewhat less marked in athletic than in sedentary individuals. These changes have implications forphysiological and medical evaluation, as well as for competitive performance. Nevertheless, mostpeople can enjoy competition to an advanced age. The sedentary person faces decreases in peakaerobic power, muscle force and endurance, flexibility and balance, with a progressively diminishedability to undertake the activities of daily living. Regular athletic participation is helpful in retardingfunctional loss. Although continuing sport participation may have little impact on longevity,enhanced function extends the period of independent living, enhancing quality-adjusted lifeexpectancy. The interpretation of physiological and medical data is sometimes difficult in olderathletes, as test results often show features that would be regarded as abnormal in a younger person.Nevertheless, a slow but progressive increase in training intensity and duration is a very saferecommendation for most older people, and it should increase rather than decrease the individualsquality-adjusted life expectancy.In sports where maximal aerobic power and flexibility are of primary importance, competitiveperformance declines progressively from early adulthood; thus, the first category of Mastersswimmers is aged 19–24 years, with additional categories established for every 5 years of agethrough the 90–94 year age category. In contrast, in sports that demand specific skills andexperience, performance may improve through to late middle-age; thus, a Masters category of golfcompetition is first distinguished for those over 50 years of age. Such categories contrast sharplywith the conventional gerontological classification of sedentary people, where distinction is drawnbetween the young old (those with little overt loss of function, typically aged 65–75 years), themiddle old (those who are experiencing some physical limitations when performing daily activities,typically aged 75–85 years) and the very old or frail elderly (typically, those over 85 years of age; afew in this age group remain healthy and very active, but many are by then severely incapacitated orconfined to institutions).Some athletes face substantial physical limitations by the age of 85 years. Others continue sportparticipation into their 90s, although because of a decreased number of registrants and changingattitudes towards events, the intensity of competition is usually decreased among olderindividuals.In this chapter, we will first examine the physiological basis of the functional losses associated withaging, and the potential to slow or even reverse these changes by an appropriate conditioningprogram. We will then look at the influence of an active lifestyle on longevity, health and qualityadjusted life expectancy. Finally, we will discuss the impact of aging upon clinical andphysiological evaluation, and the advice that a physician should offer to older individuals who wishto participate in Masters competitions.Box 9.1 Key PointsHow old is old?Sports demanding endurance and flexibility: • Age categories start at 19 yearsSports demanding specific skills: • Age categories start at 50 years
Chronic illness including chronic diseases of lifestyle will sadly affect most human beings at somepoint in their lifetime. Indeed, the burden of chronic illness and disability has a large global impacton health resources both with respect to financial and resource demand. Over the past 10 years, ithas become apparent that chronic physical activity in the form of exercise training has not only theability to prevent or delay the onset of illness and disease (primary prevention) but also forms animportant part of the management of such illness (secondary prevention). The chronic medicalconditions where exercise has been shown to be of benefit are listed in Table 11.1 .Table 11.1 -- Exercise in the Prevention and Management of Chronic Disease StatesExercise Aids in Prevention Exercise Helps in ManagementCoronary artery disease Coronary artery diseaseHypertension Heart failureObesity HypertensionStroke ObesityDiabetes (Type I) Diabetes (Type I)Breast cancer Diabetes (Type II)Ovarian cancer OsteoporosisCervical cancer Rheumatoid arthritisColon cancer OsteoarthritisOsteoporosis DepressionDepression Pulmonary diseaseLower back pain Lower back pain Chronic renal failure Acquired Immune Deficiency Syndrome Chronic fatigue syndrome and fibromyalgiaWith the advent of the data supporting physical activity in the management of chronic illness andthe subsequent publication of official position stands and statements by numerous professionalbodies advocating the use of physical exercise in the management strategies, so the growth ofprofessionals in the field of exercise science and sports medicine has occurred. Thus globally, sportsphysicians, physical therapists, biokineticists, exercise physiologists and athletic trainers haveembraced this domain of intervention and from many postgraduate training programs have emergedteaching specific techniques and approaches to chronic illness management. Indeed, in manycountries some aspects of exercise and positive lifestyle interventions have been included in theundergraduate training of primary care doctors.While in-depth discussion and guidelines for exercise rehabilitation are beyond the scope of thischapter, the reader with an interest in this topic is referred to more detailed publications on thistopic including ‘ACSMs guidelines for exercise training for patients with chronic diseases anddisabilities’ and available Position Statements from authoritative bodies.      The aim of thischapter is to outline some of the more common chronic illnesses where exercise plays an importantrole in the intervention and to advise the reader of how to formulate an exercise program for suchpatients, and provide some practical guidelines for exercise prescription and monitoring of suchpatients.
Americans made 629 million visits to CAM providers in 1997, exceeding the total number of visitsto primary care physicians. The same survey estimated that US$27 billion was spent on CAM thatyear, comparable to the out-of-pocket expenditures for all physician services in the US in 1997.The most common diagnoses for which patients sought CAM in these surveys were back pain,headache, depression and anxiety.The most comprehensive information on CAM use was gathered by the National Center for HealthStatistics (NCHS) as part of the National Health Interview Survey ( Fig. 23.1 ). As part of thisstudy, tens of thousands of Americans were interviewed about their experiences with health andillness. The 2002 version, which was completed by 31 044 adults, included detailed questions onCAM. This survey found that 36% of adult Americans had used some form of CAM, excludingmegavitamins and prayer for health reasons, in the last 12 months. People who were more likely touse CAM included women greater than men, those with higher educational levels, those who hadbeen hospitalized in the last year, and former smokers more than current or never smokers.Figure 23.1 Percentage of adults aged ≥18 who used complementary and alternative medicine (CAM) for health reasons during thepreceding 12 months, by gender in the US in 2002. (Modified from the National Center for Health Statistics.)One difficulty in surveys of CAM use is that the definition of CAM may vary. The National Centerfor Complementary and Alternative Medicine (NCCAM) has defined CAM as diverse healthcaresystems, practices and products that are not currently considered to be part of conventional medicaltraining and practice. While scientific evidence has begun to accumulate regarding some CAMtherapies for certain diagnoses, important questions regarding most of these approaches remainunanswered. The list of treatments that are considered to be CAM will continue to shift as certainCAM therapies are shown to be effective and are accepted into mainstream practice.Despite the strong interest in CAM therapies among the general population, the numbers of athleteswho make use of CAM are not known. There have been no large-scale observational studies ofCAM use by athletes published in the medical literature. The few small surveys available havefocused on specific CAM modalities, such as nutritional supplementation and chiropractic care,rather than on more general information relating to CAM use.