Exercise and illness

Chapter 7 Exercise and illness


Dysfunction of the respiratory system plays an integral role in performance during exercise. It may well be that some of these symptoms are not attributable purely to respiratory pathology and there may be either an alternative or an overlap diagnosis with cardiac disease. Breathlessness is a common symptom during exercise, especially when the patient is sub-optimally fit or exercising intensely. However, if the patient complains of excessive shortness of breath or difficulty breathing, particularly at rest or at low intensity exercise, then there may be a pathological condition going on. It may also be that the patient complains of difficulty in breathing when performing some exercise that they do not normally have any trouble with and this may become more apparent in different environmental conditions.

The most common cause of breathlessness is exercise-induced asthma. However, there may be other causes which need to be excluded and these include respiratory infections, spontaneous pneumothorax or foreign body aspiration as well as chronic obstructive airways disease. Non-respiratory causes such as cardiac ischaemia or valve disease, pulmonary embolus and anaemia as well as obesity and psychological causes need to be excluded.

A diagnosis is made by taking a full history and examination and performing investigations including respiratory function tests (see below), chest X-ray, ECG and blood tests to exclude the causes mentioned above.

Difficulty in breathing is often associated with a wheeze which, by definition, is described as an expiratory noise as opposed to an inspiratory stridor, which may reflect upper airway obstruction. Wheeze is often a symptom of bronchospasm but be aware that the patient may not need to have wheeze nor difficulty in breathing to be diagnosed as asthmatic. Some asthmatics just have a cough that may be present at night time or triggered off by exercise. The nature of the cough, being productive or non-productive or being during the day or night, may have a reflection on the diagnosis and possible causes include post-nasal drip and sinusitis, reflux oesophagitis and aspiration or bronchogenic carcinoma and including the differential diagnoses mentioned above.

Some patients complain of chest pain or tightness and obviously cardiac ischaemia needs to be excluded in these patients but this may also be the exhibiting symptom of exercise-induced asthma or bronchospasm as well as symptoms that may affect the chest wall such as rib injuries, costovertebral and costosternal joint injuries, referred pain from the thoracic spine and early onset herpes zoster. Intercostal muscle injuries as well as pleuritic chest infections can also present this way.

Investigation, as listed above, is needed to make a differential.


Asthma is a chronic inflammatory disease of the airways as a result of hyper-reactivity resulting in various symptoms to include coughing, wheezing, chest tightness and shortness of breath. The cough may be dry, irritating and persistent, often worse in the morning or late at night or after exercise and this is due to a mixture of variable airway obstruction, variable reversible airway obstruction and associated inflammation within the bronchii. Allergic triggers include house-dust mite, pollens, fungi and animal allergens but other triggers also include upper respiratory tract infections, exercise and emotional triggers including stress and laughter, as well as changes in temperature and humidity. As mentioned above, the absence of a wheeze does not exclude the diagnosis of asthma.

Exercise-induced asthma (EIA) occurs when there is bronchospasm rather than mucus overproduction and inflammation as a result of exercise. Most commonly, this occurs at the completion of exercise rather than during it and it is the exercise that triggers the bronchospasm rather than any other allergic trigger. It is estimated that 10% of the general population have symptoms associated with exercise-induced asthma and it is possible for an asthmatic to have exercise-induced asthma as well as his background asthma.13

The pathogenesis of exercise-induced asthma is controversial and may be a result of change in humidity or temperature of inhaled air. During exercise, most athlete’s mouth-breathe, thus bypassing the normal humidification processes that occurs in the nose. This results in relative dehydration of the inhaled air which seems to trigger off bronchospasm.

Asthma and exercise-induced asthma are diagnosed through respiratory function tests. The simplest test of this is measuring FEV1; the amount of forced expiratory volume within 1 s, as measured by a spirometer. By definition, asthma and exercise-induced asthma are reversible airways obstruction and so with both of these, one would expect to see a reduction in the FEV1 of greater than 12%, with exercise only to be reversible with bronchodilators such as salbutamol. The degree of drop in FEV1 or peak expiratory flow rate, as measured on a peak flowmeter, reflects the severity of the asthma. Other forms of diagnostic criteria include a eucapnic voluntary hyperpnoea test, which involves hyperventilation with dry air containing 0.9% carbon dioxide at varying levels of maximum voluntary ventilation and demonstrating a drop of FEV1 by more than 10%, which is then reversible again on the use of a bronchodilator.

Various studies have shown that anything between 9% and 15% of athletes are shown to have an undiagnosed exercise-induced asthma.

Treatment of asthma includes management of the inflammatory component, usually by a corticosteroid inhaler, and reversing the bronchospasm with bronchodilator inhalers. Both these medications need to be notified through a therapeutic usage exemption (TUE) form or declaration of use notification for the use of drug testing.

Management of exercise-induced asthma, however, involves the avoidance of exercising in a dry or cold environment, although this is not always possible. The use of masks or nose-breathing regimes have proved less effective. It is important, perhaps, that there is gradual warming up towards 80–90% of maximum intensity, so as to decrease the change in environmental factors affecting the airways; however, the mainstay of the treatment is the use of bronchodilators within the first 15 min of activity to try and counter the bronchospasm. If this is ineffective, then the use of alternative treatments, including inhaled corticosteroids, leukotriene receptor antagonists and long-acting beta-agonists, have been used.


There are always concerns when advising patients with cardiovascular disease as to how they should best exercise, and, before giving advice, it is important to understand what changes occur in the cardiovascular system with exercise.

With exercise, the heart responds by increasing its rate and contractility and with long-term exercise, resistance training can lead to pressure overload, whereas endurance training can lead to volume overload.

With pressure overload there is an increase in septal and free wall ventricular thickness, whereas in volume overload, such as in distance running athletes, there is left ventricular end diastolic diameter increase with a proportionate increase in the ventricular wall thickness.

Patients who combine weight training with endurance have a mixture of these two changes. As a result, athletes may present with a heart that is either normal size but has thickened walls or has a larger sized ventricle with a proportional increase in wall thickness or a combination of the two. It is obviously important to distinguish these changes from both pathological changes and, likewise, it is the changes that are not uncommon on examining an athlete. It is not unusual to find a slow resting pulse and an increased left ventricular size with an apex beat displaced laterally in a normal athlete. Systolic murmurs are not uncommon but it would be abnormal to find a raised blood pressure, a raised JVP or peripheral oedema. Likewise, ECG changes are not uncommon in an athlete, with sinus bradycardia and left ventricular hypertrophy being regarded as normal in 80% of athletes, and ST segment elevation is not uncommon. However, other rhythm abnormalities such as atrial fibrillation or heart block cannot necessarily be attributable to the patient being an athlete.

Bearing this in mind, what symptoms would be regarded as abnormal in an athlete when they may have cardiovascular disease?

Symptoms of palpitations, chest pain or syncopal attacks or dizzy attacks would be regarded as abnormal. Likewise, a family history or a history of murmurs needs to be investigated.


It is important when a patient presents with palpitations to be absolutely sure that this is what they are describing and not some fasciculation in their chest wall muscles or a feeling of anxiety. Other cardiac symptoms, such as chest pain, dizziness and syncope, need to be excluded and then if you are sure that they have palpitations you need to determine their onset, their triggers, their duration and whether they are regular or irregular in nature.

A history of medication, recreational drug abuse, eating disorders or other cardiac events needs to be excluded as well as other triggers, such as thyroid disease, hypoglycemia, caffeinated drinks and ephedrine. Remember that some athletes take pseudoephedrine or caffeine as a pick-me-up before competing and these can stimulate the heart.

Examination must exclude thyroid disease, cardiac murmur or an arrhythmia. Chest X-ray and ECG are helpful but it may be that the athlete needs to precipitate an attack with an exercise regime using an exercise test on a treadmill or wearing a halter monitoring system. If an abnormal exercise test results, then an echocardiogram needs to be performed to exclude an underlying structural abnormality. It is beyond the boundaries of this book to go into the treatment of cardiac arrhythmias but it is important to be aware that no cardiac structural abnormality should be omitted. It is also worthwhile being aware that the treatment for some of the cardiac arrhythmias includes beta blockers which are on WADA’s list of banned substances in certain sports, as by reducing the cardiac rate they may provide an advantage in precision sports such as shooting.

Syncope or dizzy attacks

Syncope is the loss of postural tone with an inability to stand upright and loss of consciousness brought about by reduction in cerebral blood flow due to reduced cardiac output. It is often associated with nausea and vomiting and the patient often looks pale or grey with cold sweat. The symptoms are similar when the patient is anaemic or hypoglycemic or when there is cerebral ischaemia such as from TIAs. However, it can occur with cardiac output abnormalities resulting in postural hypotension. It is important to determine whether this occurs during or after sport as syncope or fainting immediately after an event could be due to pooling of blood in the lower limbs because of absence of muscle contractility and the muscle pump pushing the blood back into the heart, reducing cardiac output and this has been labelled as exercise-associated collapse.4

Treatment is with head down and leg elevation and recovery is quick; however, if the athlete has syncopal attacks during sporting activities this can indicate a medical problem and should be taken seriously. A full history including family history of cardiac events or sudden death at a young age and a history excluding diabetes, valvular disease and hypertension needs to be excluded as well as other symptoms of cardiac disease as mentioned above. A full cardiac examination and investigations including chest X-ray, ECG, exercise stress testing echocardiogram need to be performed.

Syncope can easily be dismissed as a dizzy attack or a funny feeling and sometimes this can be confused with vertigo or hypoglycaemia. It is important for the doctor to be aware that this can be the one and only symptom that the athlete can complain of that can give you a pointer towards some underlying cardiac abnormality and it is vital to be alert to this symptom and to investigate it appropriately.

Sudden cardiac death

Sudden cardiac death related to exercise is fortunately not common but often has a high profile, as it is so tragic in occurring in otherwise fit and healthy athletes.57

Although exercising substantially reduces the risk of cardiac death, in those who are susceptible, intense exercise may increase their particular risk. Sudden death is divided into two age groups: those under the age of 35 who show evidence of a structural, congenital cardiovascular lesion and those over 35 who die of coronary artery disease. Sudden death in the young is a tragic event and in several countries around the world there are screening programmes to identify those at risk. Within the UK, CRY (Cardiac Risk in the Young) is a society that provides advice, screening and counselling for those who are at risk from this condition.

Unfortunately, there are many athletes whose first symptom of cardiac disease is their sudden death and every week eight apparently fit and healthy young people die in the UK from undiagnosed heart conditions. The most common cause of sudden death in athletes is hypertrophic cardiomyopathy which accounts for 36% of deaths in one study. This condition is characterised by hypertrophy of the ventricular wall and is associated with either an obstruction or non-obstruction to the left ventricular out-flow. It is more common in males and most sufferers have no symptoms prior to the tragic event. However, of those that did have symptoms, the most common was exertional dyspnoea which should not be confused with asthma, chest pain, or palpitations as well as pre-syncope or pseudo-syncopal attacks. Patients with hypertrophic cardiomyopathy have a jerky, carotid pulse with a double or triple apex beat associated with a cardiac murmur. There is often a fourth heart sound but otherwise examination may be normal. ECG shows evidence of left ventricular hypertrophy, ST segment changes and prominent Q waves, although, as said previously, these signs may be found in a normal athlete. However, a normal ECG makes a diagnosis of hypertrophic cardiomyopathy unlikely.

Diagnosis is clinched through an echocardiogram showing a hypertrophied non-dilated left ventricle with an absolute thickness of the left ventricle wall greater than 15 mm. It is this measurement that determines the difference between a hypertrophic cardiomyopathy and an athlete’s heart and it is important that the echocardiogram is performed by an experienced ultrasonographer. CRY offer screening programmes to adolescents and this is a service that is being increasingly used whereby the athletes are given a questionnaire exploring symptoms and family histories and then arranged to have an examination and an ECG. Those that have any positive answers on questionnaires, examination or have some abnormalities on ECG are offered an echocardiogram. In Italy, all children have to have this screening test to be allowed to proceed to a sport in their team; however, it is a highly expensive screening programme with very little pick-up unless you are the athlete that is found to have this condition.

As a sports physician, it is important to be aware of the warning symptoms so that these patients can be identified and investigated appropriately.


It is well known that exercise can bring about some physiological changes in the gastrointestinal (GI) tract, such as alteration in gastric emptying and intestinal mobility, as well as variation in blood flow to the GI tract. As a result there can be an association with variation in appetite, an increasing incidence of heartburn, reflux oesophagitis and chest pain, associated with belching, vomiting and nausea. There can be increased intestinal hurry with diarrhoea, abdominal cramping and, at times, rectal bleeding.


Under this umbrella, the symptoms of nausea, vomiting, reflux, heartburn, belching and trapped wind can be included. It is well known that patients, who have these symptoms without exercise, tend to get an exacerbation with exercise. It is important to be absolutely sure that these symptoms are, first confined to the GI tract and are not a symptom of cardiovascular or respiratory cause of chest pain, such as ischaemia, arrhythmia or respiratory dysfunction, in addition to excluding any musculoskeletal cause in the chest, such as costosternal joint dysfunction or referred pain from the thoracic spine. Be aware that the gastric emptying rate may be increased with exercise, although other factors, such as meal volume and content, as well as a level of anxiety within the athlete can play a role. It is therefore important to reduce the distention of the stomach during exercise and, if possible, one should avoid solid food for 3 h before intense exercise and the pre-match meal should be high in carbohydrate and low in protein and fat. Antacids, H2 receptor antagonists and even PPIs play a role in reducing the acidity within the stomach. Likewise, domperidone 1 h before meals can be effective. Be aware that some athletes take antiinflammatories, either long-term or before exercise or competition and this may have a negative effect on dyspepsia.9

GI bleeding, whether it is from the upper GI tract or lower GI tract, must be taken seriously, and pathological conditions excluded before it is presumed it is due to exercise. Alterations in blood flow affecting ischaemic colitis as well as the effect of antiinflammatories can all result in rectal bleeding, which should be investigated. Also, remember that chronic low level asymptomatic GI bleeding can result in anaemia and low ferritin levels, which can be a cause of decreased performance and fatigue. Serum ferritin levels of less than 30 ng/mL in women and 50 ng/mL in men indicate reduced iron stores.

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Jul 18, 2016 | Posted by in SPORT MEDICINE | Comments Off on Exercise and illness

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