3. Anaerobic processes of ATP generation
During muscle contraction, ATP is the direct connecting link between fibre shortening (or
lengthening), force development and metabolism. In this process, the ATP turnover in muscle is
most significantly determined by the quantity of calcium released from the transverse tubular
system. The most important regulatory enzymes responsible for energy release from ATP are
ATPase like actomyosin-ATPase, Na+/K+-ATPase and sarcoplasmatic reticulum Ca2+-ATPase
which, in turn, are activated by calcium. The maximum quantity of ATP that can be hydrolyzed
during a single contraction depends on the myosin isoenzyme pattern and, therefore, on the type of
muscle fibre. In addition, muscles contain phosphocreatine (PCr), which is another high-energy
phosphate 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 immediately
stimulates the breakdown of PCr to provide energy for ATP resynthesis. This reaction is catalyzed
by the enzyme creatine kinase (CK):
In other words, a fall in the ATP concentration is buffered by PCr, and therefore the ATP
concentration in the muscle remains nearly constant at a high level during physical exercise. Even
under extreme physical strain leading to exhaustion, the ATP concentration rarely falls below 50%
of the baseline value.[2] The ‘high energy phosphate’ system, however, is limited by the fact that the
quantity of releasable phosphate for the energy-production from the high-energy phosphates (PCr
and ATP) during high intensive work is drastically reduced. During short-term intensive physical
exercise 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 for
resynthesis depends on the oxidative capacity of the respective system.[3] In contrast, at highly
intensive physical loads of longer duration, the PCr concentration drops rapidly and drastically. In
this case, the resynthesis occurs through the anaerobic energy provision from carbohydrates, which
leads to the production of lactic acid, a process named anaerobic glycolysis, because this process
does not require oxygen.
Glycolysis from glycogen:
An increase in pyruvate, NADH/NAD+ ratio or H+ are metabolic changes that will promote lactate
formation. Oxygen deficiency, increased recruitment of fast twitch fibers and low aerobic
conditions in the exercising muscle are conditions for this metabolic imbalance. NADH + H+ can be
re-oxidized only by the reduction of pyruvate, catalyzed by lactate dehydrogenase (LDH). Lactic
acid is produced in this process. The process of NADH - H+ re-oxidation through pyruvate is a very
uneconomical interference because only three moles of ATP are obtained from the degradation per
mole glycosyl unit, whereas 36 moles/38 moles of ATP can be formed during complete oxidation.[4]
Glycogen phosphorylase plays a key role in anaerobic glycolysis. It breaks down the muscle
glycogen and is regulated by Ca2+ released from the transverse tubular system through the enzyme
phosphorylase-kinase. Generally, the reduced Ca2+ release from the tubular system during
cumulative fatigue is an indication of the importance of Ca2+ in muscle fatigue. Also the enzyme
phosphofructokinase, 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 anaerobic
glycolysis in the sense that it is inhibited by the sinking pH value due to the lactic acid production
and thus limiting the anaerobic glycolysis. In fact, H+ ion concentrations influence glycolysis and
the PCr concentration during physical exercise. [3] [5] A high H+ concentration reduces the PCr level
through the enzyme creatine kinase. Furthermore, local acidosis in the working muscles appears to
4. further reduce the formation of cross-bridges between the myosin heads and the actin molecules of
muscle fibers. In this context, it should be mentioned that a metabolic acidosis is not an absolute
prerequisite for muscle fatigue because patients with a congenital glycogen phosphorylase
deficiency (McArdle's disease) are prone to early fatigue despite the fact that they have no lactate
acidosis.[6]
During high intensive exercise, lactic acid can be accumulated for two reasons. As a result of the
extremely high glycolysis rate which occurs under intensive physical strain, pyruvate is formed in
such 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 a
sufficient rate by the mitochondrial membrane. When very intensive exercise continues to persist,
which requires continued anaerobic energy production, the buffer capacity of the organism is
exceeded and lactic acid accumulates. Based on these theoretical considerations, the concentration
of 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 most
important parameters to determine endurance performance and also to optimize the training
processes ( 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 load
steps, the blood lactate concentration as an indirect measure of the lactic acid produced in the
exercising muscles remains stable because the energy demand, meaning the ATP-resynthesis rate is
met by oxidation of fats and carbohydrates. Although at the beginning of the exercise or when
increasing the workload step by step, lactate will be produced in the working muscles because of
the delay of the cardio-respiratory supplying reactions, lactate will be metabolized within the
muscles and will not be carried to other compartments like blood, a process which is called ‘cell to
cell shuttle’. From a certain point, when the exercise intensity is higher, fast twitch muscle fibers
which have a lower oxidative potential and therefore produce more lactate have to be activated and
5. therefore lactate in the exercising muscles is formed and the blood lactate concentration will
increase. This point, which is called the aerobic threshold or first lactate turn point is the beginning
of a so-called ‘mixed aerobic-anaerobic metabolism’. With increasing intensity a second deflection
point can be observed, when more lactate in the exercising muscle will be produced than can be
buffered or even removed. From this point called the anaerobic threshold or respiratory
compensation threshold, or the second lactate turn point, lactate production increases rapidly, will
be 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 differences
in the interaction of the aerobic–anaerobic metabolism can easily be seen. The untrained person
shows a very rapid increase and accumulation of the blood lactate concentration from the resting
value. In contrast, in the endurance-trained marathon runner, the lactate level remains low with
increasing workloads, which is the result of the aerobic adaptations by the endurance training. That
means that both – the first and the second lactate turn points – occur at a higher percentage of the
athlete's maximal aerobic power. On the other hand, the production rate of lactic acid and resistance
against lactate accumulation is decreased. In contrast, the 400-m runner shows an earlier increase of
the lactate production because of the specific metabolic adaptations resulting from anaerobic
training. 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 the
acidification resulting from increasing lactate accumulation better as a consequence of the anaerobic
training ( Fig. 2.2 ).[7]
Figure 2.2 Lactate-performance curves and heart rate performance curves of three different trained individuals.
Aerobic processes of ATP generation
In contrast to the anaerobic energy system which provides energy at a high liberation rate but with
limited supply, muscles need a continuous supply of energy at rest and during long duration but low
intensive activities. This is provided by the oxidative (aerobic) system which has a lower energy
6. liberation rate but a tremendous energy yielding capacity. Aerobic production of ATP occurs in the
mitochondria and involves the interaction of the citric acid cycle (Krebs Cycle) and the electron
transport chain. Oxygen serves as the final hydrogen acceptor at the end of the electron transport
chain. The term maximal aerobic power (VO2max, VO2peak) reflects the amount of ATP which can
be produced aerobically and therefore the rate at which oxygen can be transported by the
cardiorespiratory system to the active muscles. From resting metabolism (3.5 ml/kg per min) the
aerobic power production can be increased up to peak values of 35–38 ml/kg per min and 42–45
ml/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 carbohydrate
The first step in the oxidation of carbohydrates is the anaerobic breakdown of muscle glycogen and
blood glucose to pyruvate. In the presence of oxygen, pyruvate – the end product of glycolysis – is
converted 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 into
carbon dioxide and hydrogen and forming two ATPs. In addition, six molecules of reduced
nicotinamide-adenine-dinucleotide (NADH) and two molecules of reduced flavin-adenine-
dinucleotide (FADH 2) are also produced from the glucose molecule, which carry the hydrogen
atoms 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 muscle
results in a net yield of about 36 or 38 ATPs depending on which shuttle system is used to transport
NADH to the mitochondria ( Fig. 2.3 ).[8]
7. Figure 2.3 ‘Flow sheet’ for energy yielding processes from lipids, carbohydrates and proteins. (Redrawn from Smekal 2004.[8])
Oxidation of fat
Fat can only be metabolized in the presence of oxygen. The triglycerides are stored in fat cells and
within 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 and
three molecules of free fatty acids (lipolysis). After having entered the mitochondria, the free fatty
acids undergo a series of reactions in which they are converted to acetyl-coenzyme A, a process
called beta-oxidation. From this point, the fat metabolism then follows the same pathway as the
carbohydrate metabolism when acetyl coenzyme A enters the Krebs Cycle and the electron
transport chain. While the ATP-amount produced varies depending on the oxidation of different
fatty acids, the complete oxidation of one (18-carbon) triglyceride molecule results in a total energy
yield of about 460 ATPs. Although triglyceride oxidation provides more energy production per
gram than carbohydrates, the oxidation of fat requires more oxygen, meaning that fat mostly is
oxidized at rest or during moderate exercise when oxygen delivery is not limited by the oxygen
transport system. At rest, e.g. the ratio of ATP-production is up to 70% of fat and 30% from
carbohydrates, whereas during high intensity exercise, the majority of energy or even the total
energy comes from carbohydrates.
8. Oxidation of proteins
Oxidation of proteins is also utilized to obtain energy at rest as well as during physical exercise.[9]
Several amino acids (especially leucine, isoleucine, alanine and valine) contribute to the production
of energy. The access to amino acids increases in proportion to the load intensity of any physical
activity, but the proportion of energy provided by amino acids during physical exercise appears to
be limited to about 10%. However, of practical significance is the fact that amino acids are oxidized
in greater quantities when the caloric supply is insufficient and also in the presence of a
carbohydrate deficiency. This leads to catabolic states (degradation of functional proteins) and loss
of nitrogen. The degradation of functional proteins is problematic because muscles are affected by
this phenomenon, which obviously has a detrimental effect on performance capacity.[10]
Power and capacity of energy yielding processes
An important approach to a better understanding of energy demand and energy supply during
physical activity and sports is the question as to which substrates are utilized for the production of
energy at specific intensities. An important factor in the selection of the substrate is the rate at
which energy can be released from the respective substrate, i.e. the maximum achievable release of
energy 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 capacity
is limited to only 3–7 s and therefore needs to be replenished constantly providing other processes
for ATP resynthesis on a lower energy liberation rate, the glycolytic (anaerobic) and the oxidative
combustion of fuels.
The glycolytic pathway can provide energy rapidly because of the high concentration of glycolytic
enzymes and the speed of the chemical reactions involved. However, glycolysis cannot supply as
much energy per second as the ATP-PC system. At high intensity exercise, the highest energy
liberation from glycolysis occurs during the first 10–15s because acidification of muscle fibers
reduces the breakdown-rate of glucose and glycogen. This impairs glycolytic enzyme function and
decreases the fiber's calcium binding capacity and thus muscle contraction. This causes an increase
of the muscle lactate up to more than 25–30 mmol/kg wt, and later one of blood lactate up to 18–25
mmol/l ( Table 2.1 ).[1]
Table 2.1 -- Power and Capacity of Energy Yielding Processes in Human Muscle
Power (mol ATP/min) Capacity (mol/ATP)
Pcr 2.5 0.37
Lactate 1.9 0.94
CHOox 1.1 59
FFAox 0.6 Not limited
Pcr, phosphocreatine; CHOox, carbohydrate oxidation; FFAox, free fatty acid oxidation. For
details, see Henriksson and Sahlin 2002.[1]
The muscle cells capacity for anaerobic glycolysis during maximal physical activity is for a period
of 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
9. energy production at the beginning of less intense exercise, when oxygen uptake kinetics lag behind
the total energy demand placed on the system.
Stored carbohydrates supply the body with a rapidly available form of energy with 1 g of
carbohydrate yielding approximately 4.1 kcal (17.1 kJ) of energy. Under resting conditions, muscle
and liver take up glucose and convert it into a storage form of carbohydrate, called glycogen, which
is, when needed as an energy source, broken down into glucose and can be metabolized to generate
ATP anaerobically and aerobically.
The carbohydrate stores of the human organism are limited. They are composed of the circulating
glucose in blood, and carbohydrates which are stored in the form of glycogen in the muscle and
liver. The quantity of carbohydrates which can be stored in the form of glycogen in the skeletal
muscles depends on a number of factors (e.g. nutrition, the state of training, muscle mass, the
composition of muscle fibers and several other factors). Therefore, published data about the
quantity of stored glycogen in the entire musculature vary between 1000 and 1900 kcal or even
slightly more in trained athletes after carbohydrate loading. Taking into consideration that the
muscles needed for physical exercise (e.g. the marathon run or biking) only constitute a part of the
entire muscle mass, the carbohydrate reserves of the working musculature must obviously be
regarded as an important limiting factor during physical strain of long duration and/or high
intensity. 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.[8] It is important to
mention that hepatic glycogen has another important function: it maintains the supply of blood
sugar to the brain, which is also important during exercise of high intensity or long duration ( Table
2.2 ).
Table 2.2 -- Body Stores for Fuels and Energy[a]
Grams kcal
Untrained Trained Untrained Trained
Carbohydrates
Liver glycogen ∼80 ∼120 ∼328 ∼492
Muscle glycogen ∼250 ∼400 ∼1025 ∼1640
Glucose in body fluids ∼15 ∼18 ∼62 ∼74
Total ∼345 ∼538 ∼1415 ∼2206
Fats
Subcutaneous 8000 6000 74 000 55 880
Intramuscular 50 300 465 2790
Total 8050 6300 74 465 58 670
Amino acids 100 110 410 451
Proteins 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 high
intensive loads requiring more than 70% of the maximum oxygen uptake. Compared with the
anaerobic energy breakdown, the rate of energy liberation with the oxidation of carbohydrates is
about one half and its capacity depends on the amount of glycogen stored in the muscles and in the
liver. Without any substitution of carbohydrates during a long duration exercise, carbohydrate
10. capacity allows endurance exercise for about 60–90 (120) min depending on the involved muscular
system and the intensity of the physical activity.
Because muscle glycogen stores are limited and can become depleted during longer lasting vigorous
exercise, an adequate diet especially for endurance exercise must contain a reasonable amount of
carbohydrates, which enhance glycogen synthesis and also glycogen stores in muscles and liver.[11]
Fats are stored well in the organism but oxidized rather slowly. In order to utilize fat from fat
deposits as a source of energy, they must be mobilized and transported to the muscle cell in the
blood in the form of free fatty acids, bound to albumin. However, fats are also present within the
muscle 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 free
fatty acids in plasma. If the intensity of physical activity is increased further, intramuscular fats and
carbohydrates are utilized in greater measure to fulfill the energy requirements. Fat oxidation does
not increase at higher load intensities, but it is rather markedly reduced. A large body of data shows
that the limitation is particularly within the mitochondria. This is also evidenced by the fact that the
oxidation of intramuscular fats seems to occur in an incomplete fashion. The most likely theory at
the present time points to a blockade of the transport of long-chain fatty acids through the inner
mitochondrial membrane when the rate of glycolysis is high (high intensity load). However, it is
evident that in the presence of a markedly increased oxidative capacity of mitochondria, which is
found in persons who have undergone endurance training, larger quantities of metabolites resulting
from beta-oxidation can be oxidized. In other words, at the same load intensity, less metabolites are
formed during glycolysis – which, in turn, has a positive effect on fat oxidation ( Fig. 2.4 ).[12]
Figure 2.4 Total energy supply and relation of fat and carbohydrates during incremental workload. (Estimated from data by Achten and
Jeukendrup 2003.[12])
As discussed earlier, even in persons with a very good endurance performance, the energy flow rate
from fat is limited. If one assumes that the energy requirements for various sports increase with the
load 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
13. In the ancient Olympic Games, at the end of the third century BC, according to Galen and other
authors of the time, athletes believed that drinking herbal teas and eating mushrooms could increase
their performance during the competitions.[3] Another interesting form of doping of this time was to
prepare a powder with the oil, dust and sweat adhering to the skin of the athlete after the
competition. This mix was removed in the dressing room with the ‘strigil’, a metallic instrument
with the shape of an ‘L’ as show in Figure 4.1 . The athlete sold it to other participants, who
believed 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 Ancient
Olympia.[4]
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 to
strychnine and cocaine, were used to increase performance. Spanish writers report a use from the
Incas of chewing coca leaves, to help cover the distance between Cuzco and Quito, in Ecuador.[5] In
1886, the first fatality caused by doping was reported, when a cyclist named Linton died after an
overdose of stimulants in a race between Bordeaux and Paris.[6]
16. role in oxygen transport. Inadequate iron intake, absorption or excessive loss limits the amount of
iron available for this and other intracellular processes.[2]
Iron deficiency anemia is common in non-athletic populations and is likely the most common
nutritional deficiency in the western world. The issue of whether iron deficiency is more common in
athletes has always been a point of controversy. Large studies have shown that iron deficiency
occurs in about 20% of menstruating women and 1–6% of postmenopausal women and men.[3]
Some studies have shown a higher prevalence of iron deficiency in female athletes than the general
population, while others have failed to show a difference when compared with proper controls. [4] [5]
This suggests that exercise itself is not a risk factor for the condition, but athletes may be more
prone to developing it.
Pseudoanemia, although not a true anemia, is the most common anemia in endurance athletes. As
mentioned in earlier, endurance athletes tend to have lower Hb levels than the general population
despite a normal red cell mass. This is due to an expansion of plasma volume and a subsequent
dilutional effect. This ‘sports anemia’ due to dilution of RBCs is referred to as pseudoanemia and is
an adaptation of exercise and does not seem to inhibit athletic performance. It is not a pathologic
condition and it normalizes with training cessation in 3–5 days. The Hb level in a well-conditioned
athlete may be 1–1.5 g/dl lower than the laboratory quoted ‘normal’. The physician looking after
athletes 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 pathological
anemias.
Footstrike hemolysis refers to the bursting of RBCs in the circulation, from the impact of
footfalls.[1] Rowing and swimming also have been shown to have similar intravascular hemolysis
and hence, such destruction of RBCs may be due to exertion as opposed to the footstrike itself.[6]
This hemolysis is usually mild and rarely if ever drains iron stores and causes anemia. Diagnosis
can be made when one has the combination of an elevated red cell volume, reticulocytosis and a
low 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 is
unknown at this point how to treat hemolysis from non-impact sports, however, since it is so mild,
treatment is rarely required.
Relation to sport
The underlying development of iron deficiency anemia is either due to blood loss or poor iron
intake through diet. Other sources have been suggested but do not appear to contribute to a
clinically 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 footstrike
hemolysis; none of these appear to deplete iron stores in sufficient amounts to cause anemia.[2] The
main culprit then seems to be dietary in nature. Athletes, especially women, involved in sports such
as long-distance running, ice skaters and gymnasts, through restrictive diets, consume too little iron
to meet their daily needs. Vegetarian athletes are particularly at risk because the iron in vegetables
and grains is not as readily absorbed as that in red meat.
Signs and symptoms
Athletes with iron deficiency anemia may be asymptomatic, while others may experience muscle
weakness, palpitations or shortness of breath. They usually seek medical attention because of
fatigue or decreased performance.[2] A complete history should be taken to rule out significant GI or
GU sources, although this is uncommon in a younger population, it may be significant in older
athletes.
Investigations
19. Aging is associated with a progressive decline in most biological functions, but changes are
somewhat less marked in athletic than in sedentary individuals. These changes have implications for
physiological and medical evaluation, as well as for competitive performance. Nevertheless, most
people can enjoy competition to an advanced age. The sedentary person faces decreases in peak
aerobic power, muscle force and endurance, flexibility and balance, with a progressively diminished
ability to undertake the activities of daily living. Regular athletic participation is helpful in retarding
functional loss. Although continuing sport participation may have little impact on longevity,
enhanced function extends the period of independent living, enhancing quality-adjusted life
expectancy. The interpretation of physiological and medical data is sometimes difficult in older
athletes, 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 safe
recommendation for most older people, and it should increase rather than decrease the individual's
quality-adjusted life expectancy.
In sports where maximal aerobic power and flexibility are of primary importance, competitive
performance declines progressively from early adulthood; thus, the first category of Masters
swimmers is aged 19–24 years, with additional categories established for every 5 years of age
through the 90–94 year age category. In contrast, in sports that demand specific skills and
experience, performance may improve through to late middle-age; thus, a Masters category of golf
competition is first distinguished for those over 50 years of age. Such categories contrast sharply
with the conventional gerontological classification of sedentary people, where distinction is drawn
between the young old (those with little overt loss of function, typically aged 65–75 years), the
middle 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; a
few in this age group remain healthy and very active, but many are by then severely incapacitated or
confined to institutions).
Some athletes face substantial physical limitations by the age of 85 years. Others continue sport
participation into their 90s, although because of a decreased number of registrants and changing
attitudes towards events,[1] the intensity of competition is usually decreased among older
individuals.
In this chapter, we will first examine the physiological basis of the functional losses associated with
aging, and the potential to slow or even reverse these changes by an appropriate conditioning
program. We will then look at the influence of an active lifestyle on longevity, health and quality
adjusted life expectancy. Finally, we will discuss the impact of aging upon clinical and
physiological evaluation, and the advice that a physician should offer to older individuals who wish
to participate in Masters competitions.
Box 9.1
Key Points
How old is old?
Sports demanding endurance and flexibility:
• Age categories start at 19 years
Sports demanding specific skills:
• Age categories start at 50 years
22. Chronic illness including chronic diseases of lifestyle will sadly affect most human beings at some
point in their lifetime. Indeed, the burden of chronic illness and disability has a large global impact
on health resources both with respect to financial and resource demand. Over the past 10 years, it
has become apparent that chronic physical activity in the form of exercise training has not only the
ability to prevent or delay the onset of illness and disease (primary prevention) but also forms an
important part of the management of such illness (secondary prevention). The chronic medical
conditions where exercise has been shown to be of benefit are listed in Table 11.1 .[1]
Table 11.1 -- Exercise in the Prevention and Management of Chronic Disease States
Exercise Aids in Prevention Exercise Helps in Management
Coronary artery disease Coronary artery disease
Hypertension Heart failure
Obesity Hypertension
Stroke Obesity
Diabetes (Type I) Diabetes (Type I)
Breast cancer Diabetes (Type II)
Ovarian cancer Osteoporosis
Cervical cancer Rheumatoid arthritis
Colon cancer Osteoarthritis
Osteoporosis Depression
Depression Pulmonary disease
Lower back pain Lower back pain
Chronic renal failure
Acquired Immune Deficiency Syndrome
Chronic fatigue syndrome and fibromyalgia
With the advent of the data supporting physical activity in the management of chronic illness and
the subsequent publication of official position stands and statements by numerous professional
bodies advocating the use of physical exercise in the management strategies, so the growth of
professionals in the field of exercise science and sports medicine has occurred. Thus globally, sports
physicians, physical therapists, biokineticists, exercise physiologists and athletic trainers have
embraced this domain of intervention and from many postgraduate training programs have emerged
teaching specific techniques and approaches to chronic illness management. Indeed, in many
countries some aspects of exercise and positive lifestyle interventions have been included in the
undergraduate training of primary care doctors.
While in-depth discussion and guidelines for exercise rehabilitation are beyond the scope of this
chapter, the reader with an interest in this topic is referred to more detailed publications on this
topic including ‘ACSM's guidelines for exercise training for patients with chronic diseases and
disabilities’ and available Position Statements from authoritative bodies. [2] [3] [4] [5] [6] The aim of this
chapter is to outline some of the more common chronic illnesses where exercise plays an important
role in the intervention and to advise the reader of how to formulate an exercise program for such
patients, and provide some practical guidelines for exercise prescription and monitoring of such
patients.
33. Americans made 629 million visits to CAM providers in 1997, exceeding the total number of visits
to primary care physicians. The same survey estimated that US$27 billion was spent on CAM that
year, comparable to the out-of-pocket expenditures for all physician services in the US in 1997.[2]
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 Health
Statistics (NCHS) as part of the National Health Interview Survey ( Fig. 23.1 ).[3] As part of this
study, tens of thousands of Americans were interviewed about their experiences with health and
illness. The 2002 version, which was completed by 31 044 adults, included detailed questions on
CAM. This survey found that 36% of adult Americans had used some form of CAM, excluding
megavitamins and prayer for health reasons, in the last 12 months. People who were more likely to
use CAM included women greater than men, those with higher educational levels, those who had
been 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 the
preceding 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 Center
for Complementary and Alternative Medicine (NCCAM) has defined CAM as diverse healthcare
systems, practices and products that are not currently considered to be part of conventional medical
training and practice.[4] While scientific evidence has begun to accumulate regarding some CAM
therapies for certain diagnoses, important questions regarding most of these approaches remain
unanswered. The list of treatments that are considered to be CAM will continue to shift as certain
CAM 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 athletes
who make use of CAM are not known. There have been no large-scale observational studies of
CAM use by athletes published in the medical literature. The few small surveys available have
focused on specific CAM modalities, such as nutritional supplementation and chiropractic care,
rather than on more general information relating to CAM use.