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== Introduction  ==
== Introduction  ==

Revision as of 08:42, 10 March 2017

Introduction[edit | edit source]

Exercise training asks many of human physiological systems in order to maintain homeostasis, this is the inner balance of the body.[1]
While exercising homeostasis is endangered by the increased amount of O 2 and nutrients demand,the need to get rid of CO 2 and metabolic waste products, rising body temperature and acid imbalance and varying hormone levels.[1]

Acute Adaptations to Exercise[edit | edit source]

Cardiovascular Responses[edit | edit source]

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 direclyt proportional to the oxygen consumption of skeletal muscles.

Cardiac Output[edit | edit source]


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.

Blood Pressure[edit | edit source]

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 systolic blood pressure raise should prevent excessive blood pressure drop which would be triggered by a decreasing peripheral resistance. The peripheral resistance of blood flow is formed from the constriction of the vessel volumes in the peripheral vessels. Under physical demands the vessels dilate, increasing their diameters. Hypertension patients have reduced peripheral resistance, and this results in higher average blood pressure. Two to three hours post exercise blood pressure drops below pre-exercising values, this is known as "postexercise hypotension".

Coronary Circulation[edit | edit source]

Coronary arteries supply the myocardium with blood and nutrients; on average one cappillary supplies one myocardial fibre  in the ventricular walls and papillary muscles[2].

Pulmonary System Adaptations[edit | edit source]

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.

Resistance Exercise[edit | edit source]

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. In the document “Exercise and Hypertension” (2004)[3] of the American College of sportsmedicine, the evidence for a blood pressure lowering effect in hypertensive adults of resistance training was evaluated as Evidence level B.[ Evidence level A is the highest level.]

Skeletal Muscle Fibre Type[edit | edit source]

The type of physial exercise being undertaken determines tthe predominant muscle fibre type.

Regular, longer-lasting endurance training increases the number of mitochondrials and the gas exchange capacity of the trained myofibres. In marathon runners slow-twitch fibers dominate the trained leg muscles, while sprinters possess predominantly fast-twitch fibers. 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[edit | edit source]

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.

Immunological Adjustments[edit | edit source]

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
[edit | edit source]

Skeletal Muscle Adaptations to Endurance Training[edit | edit source]

The cross-sectional area of slow-twitch fibres increases a little in response to aerobic work. Fast-twitch fibres develop a higher oxygen capacity. Trained muscles possess a higher number of capillaries then untrained muscles; this allows a greater blood flow.

Resistance Training Adaptations in Skeletal Muscle Cells[edit | edit source]

Resistance training causes increased muscle size (hypertrophy) through an increase of myofibril size and number of fast- and slow-twitch fibres. Moreover the recruitement pathway of muscle fibres become more effective. Resistance training thus leads to a greater force development of the trained muscles.

Ligament and Tendon Adaptations[edit | edit source]

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[edit | edit source]

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 and Respiratory Adaptations[edit | edit source]

Post-training heart rate is decreased at rest and during submaximal 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.
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 bloodpressure values.
Blood pressure reductions occur after short bouts of exercises of 3 minutes duration and an intensity of 40% VO2max.
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[edit | edit source]

  • Uncontrolled or poorly controlled asthma.
  • Cancer or blood disorders: when treatment or disease cause leucocytes below 0.5 x109/L, haemoglobin below 60g/L or platelets below 20 x 109/L.
  • 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 diabetic peripheral or autonomic neuropathy or foot ulcers should avoid weight bearing 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 activity8 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 embolus or pulmonary infarction. Excessive or unexplained breathlessness on exertion.
  • Any acute severe illness.

Adverse Effects[edit | edit source]

Musculoskeletal Adverse Effects[edit | edit source]

Sudden force development, or repetitive movements can lead to musculoskeletal strain, tear or fracture.

Cardiovascular Events[edit | edit source]

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 reason was hypertrophic cardiomyopathy.

References[edit | edit source]

  1. 1.0 1.1 Joseph T. Wearn. THE EXTENT OF THE CAPILLARY BED OF THE HEART. J Exp Med. 1928 Jan 31; 47(2): 273–290.
  2. Joseph T. Wearn. THE EXTENT OF THE CAPILLARY BED OF THE HEART. J Exp Med. 1928 Jan 31; 47(2): 273–290.
  3. Pescatello LS, Franklin BA, Fagard R, Farquhar WB, Kelley GA, Ray CA; American College of Sports Medicine position stand. Exercise and hypertension.Med Sci Sports Exerc. 2004 Mar;36(3):533-53.