Original Editor - Nadja Thöner
- 1 Introduction
- 2 Acute Adaptations to Exercise
- 3 Chronic Adaptations of Exercise
- 4 Absolute Contraindications to Exercise
- 5 Adverse Effects
- 6 References
Exercise training challenges many human physiological systems that need to adapt in order to maintain homeostasis, this is the inner balance of the body. While exercising, homeostasis is endangered by the increased amount of O2 and nutrients demand, the need to get rid of CO2 and metabolic waste products, rising body temperature and acid imbalance and varying hormone levels.
Acute Adaptations to Exercise
All the cardiovascular system components, heart, blood vessels and blood, are involved in the immediate response of the cardiovascular system to physical stress. During exercise, the cardiovascular response is largely directly proportional to the oxygen consumption of skeletal muscles.
Cardiac Output (Q) is defined as the amount of blood pumped by the left ventricle of the heart per minute. It is expressed as litres/minute. It is the product of heart rate (HR) X stroke volume (SV).
A person's maximum oxygen uptake (VO2 max) is the cardiac output (Q) X arteriovenous oxygen difference (A-VO2).
The arteriovenous difference is a measure for the oxygen intake from the blood as it passes the body, e.g. activated muscle cells. The unit is millimetres oxygen per 100 mL of blood. At rest the value is on average about 4-5 mL/100mL of blood and can raise progressively during an exercise up to 16 mL/100mL of blood (4).
Cardiac output multiplied with A-VO2 difference form the maximum oxygen uptake capacity (VO2max) of an individual.
With a stepping working rate, the cardiac output increases in a nearly linear fashion in order to meet the increasing oxygen demand.
Cardiac output is measured by echocardiography.
With increasing physical stress, blood flow is directed away from the internal organs to the activated muscles; at maximal rates of work, 80 percent of the cardiac output goes to the activated muscles and the skin, whereas in rest this value is just twenty percent.
There is a linear increase in systolic blood pressure to peak values of 200 to 249 mmHg in normotensive individuals, and the diastolic pressure value remains near rest level.
Hypertensive individuals reach higher systolic blood pressures at a given rate of work, and they can also reach higher diastolic values. The peripheral resistance of blood flow is related to vessel diameter and length and blood viscosity in the peripheral vessels. Under physical demands the vessels dilate, increasing their diameters. Hypertension patients have increased peripheral resistance compared to normal, and this is a major cause of their higher average blood pressure. Two to three hours post exercise blood pressure drops below pre-exercising values, this is known as "post exercise hypotension".
Coronary arteries supply the myocardium with blood and nutrients; on average one capillary supplies one myocardial fibre in the ventricular walls and papillary muscles.
Pulmonary System Adaptations
Pulmonary ventilation is initiated via the respiratory centre in the brainstem with parallel activation through the motor cortical drive that activates skeletal muscles and afferent Type III-IV muscle afferent fibres.
While maximum exercise training ventilation rates in normal-sized healthy people may increase by a factor of ten, compared to ventilation rates at rest.
Dynamic training and resistance training differ primarily in the fact that resistance training produces a vigorous increase in the peripheral vascular resistance.
In the case of resistance training, high isolated forces are generated in the activated musculature. The strong isolated muscle contraction compresses the small arteries and thus increases the peripheral vessel resistance.
Skeletal Muscle Fibre Type
The type of physical exercise being undertaken determines the predominant muscle fibre type.
Regular, longer-lasting endurance training increases the number of mitochondria and the gas exchange capacity of the trained myofibrils. In marathon runners slow-twitch fibres dominate the trained leg muscles, while sprinters possess predominantly fast-twitch fibres. Endurance training has the potential to change metabolic properties of skeletal muscles in the direction of an oxidative profile. The question as to how far muscle fibre types can be reprogrammed remains open.
Hormonal Responses to Exercise
The stress hormones adrenaline and noradrenaline (the catecholamines) are responsible for many physiological adaptation procedures through training. Catecholamines are part of cardiovascular and respiratory training adaptations, and in fuel mobilisation and utilisation.
Moderate training enhances some components of the immune system and thereby reduces the susceptibility to infections. In contrast, a reduced functionality of immune cells occurs after overstraining.
Chronic Adaptations of Exercise
Skeletal Muscle Adaptations to Endurance Training
Slow-twitch fibres: The cross-sectional area of slow-twitch (AKA red) fibres increases slightly in response to aerobic work.
Fast-twitch fibres: These fibres develop a higher oxygen capacity.
Capillary bed density: Trained muscles possess a higher density of capillaries than untrained muscle, which permits a greater blood flow with increased delivery of nutrients.
Resistance Training Adaptations in Skeletal Muscle Cells
Resistance training causes increased muscle size (hypertrophy) through an increase of myofibril size and number of fast- and slow-twitch fibres. Moreover the recruitment pathway of muscle fibres become more effective. Resistance training thus leads to a greater force development of the trained muscles.
Ligament and Tendon Adaptations
There is an increase in cross-sectional area of ligaments and tendons in response to prolonged training, as the insertion sites between ligaments and bones and tendons and bones become stronger.
Metabolic Adaptations of Prolonged Exercise
Endurance training increases the size and number of mitochondria in the trained muscle; the myoglobin content may sometimes increase, thus the oxygen storage capacity increases sometimes. In trained muscles glycogen storage capacity increases, and the ability to use fat as an energy source.
Long Term Cardiac Adaptations
When healthy individuals participate in a long term aerobic exercise programme they undergo positive cardiac adaptions, both morphologically and physiological. They have increased early diastolic filling and increased contractile strength. Morphological changes appear in both the left and the right ventricle. The cardiac adaptations lead to increased cardiac output while exercising, and a higher VO2max after exercise
Post-training heart rate is decreased at rest and during sub-maximal exercise. Stroke volume increases through long term endurance training. Endurance training increases plasma volume, which elevates the blood volume that returns to firstly the right heart and after that to the left ventricle. The greater amount of blood in circulation causes an increase in the amount of blood in the left ventricle when the end-diastolic phase is reached. The end-diastolic phase is the phase in which the passive filling (diastole) of the heart finishes. The left ventricle is fully filled and its wall is stretched. The passive stored energy in the wall helps to a forceful contraction in the emptying phase (systole). As a result the heart muscle is hypertrophied. Each heart muscle fibre increases in size. The hypertrophy refers to the ventricle and the posterior and septal walls.
High blood pressure = systolic blood pressure ≥140 and/or diastolic blood pressure ≥90 mm Hg blood pressure. The positive correlation of blood pressure and cardiovascular disease (CVD) risk starts from 115 mm Hg systolic and 75 mm Hg diastolic and doubles with every 20 mm Hg systolic and 10 mm Hg diastolic increase. According to the American College of Sports medicine, dynamic aerobic training reduces blood pressure (BP) in Individuals with hypertension. Hypertension is a risk factor for cardiovascular events. Endurance exercises lower arterial blood pressure for some hours after a bout of exercise: this phenomenon is the post-exercise hypotension. Post-exercise hypotension seems to be greater in people with higher pre-exercise blood pressure values.
Blood pressure reductions occur after short bouts of exercises of 3 minutes duration and an intensity of 40% VO2max.
Morphological cardiac adaptations is less in people with cardio vascular disease than when compared to younger, healthy people. 
Long Term Respiratory Adaptations
The blood flow in the upper regions of the lungs increases after prolonged endurance training and the respiration rate increases.
Absolute Contraindications to Exercise
- Uncontrolled or poorly controlled asthma.
- Cancer or blood disorders: when treatment or disease cause leukocytes below 0.5 x109/L, haemoglobin below 60g/L or platelets below 20 x 109/L. If a patient has a platelet count of <20 000 then only AROM and ADLs are advices due to the increased risk of bleeding, 20 000-30 000: light exercise only.
- COPD: Patients are required to be stable before training and oxygen saturation levels should be above 88-90%.
- Diabetes: If blood glucose is >13 mmol or <5.5 mmol/l then it should be corrected first.8 Patients with severe diabetic peripheral or autonomic neuropathy or foot ulcers should be assessed before undertaking exercise. Any diabetic with acute illness or infection.
- Heart disease: acute myocardial infarction or unstable angina until stable for at least 5 days, dyspnoea at rest, pericarditis, myocarditis, endocarditis, symptomatic aortic stenosis, cardiomyopathy, unstable or acute heart failure, uncontrolled tachycardia.
- Hypertension: resting blood pressures of a systolic >180 or diastolic >100 or higher should receive medication before regular physical activity with particular restrictions on heavy weights strength conditioning, which can create particularly high pressures.
- Osteoporosis: avoid activities with a high risk of falling.
- Fever: should be settled to avoid a risk of developing myocarditis.
- Unexplained dizzy spells.
- Acute pulmonary embolism or pulmonary infarction. Excessive or unexplained breathlessness on exertion.
- Any acute severe illness.
Musculoskeletal Adverse Effects
Sudden force development, or repetitive movements can lead to musculoskeletal strain, tear or fracture.
In an epidemiological study, Prevalence of Sudden Cardiac Arrest (SCA) was studied between 2002-2013 and was compared with medical data in the USA. Of 1,247 cases of SCA, 63 were occurred during sport activities. The affected persons were 51.1 ±8.8 years old. The incidence is 21.7 (95% -CI 8.1-35.4) per million per year and varies based on sex for sports SCA. Men possess a Risk Ratio of 2.58 (95%-CI 2.12-3.13)
Another study investigated the US National Registry of Sudden Death in Athletes. They found a total of 2406 deaths between years 1980-2011. The young athletes were 19 ±6 years old and were engaged in 29 diverse sports. Young men were affected 6.5 times more frequently than women. The most common reason was hypertrophic cardiomyopathy.
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