Exercise Physiology: Difference between revisions

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<span style="font-size: 13.28px;">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.</span>  
<span style="font-size: 13.28px;">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.</span>  


=== Resistance Training Adaptations in skeletal muscle cells ===
=== 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 recruitement pathway of muscle fibres become more effective. Resistance training thus leads to a greater force development of the trained muscles.<br>  
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.<br>  


=== Ligament and Tendon Adaptations ===
=== Ligament and Tendon Adaptations ===


There is an increase in cross-sectional area of ligaments and tendons in response to prolonged&nbsp;training, as the insertion sites between ligaments and bones and tendons and bones become stronger.
There is an increase in cross-sectional area of ligaments and tendons in response to prolonged&nbsp;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&nbsp;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.


== References  ==
== References  ==

Revision as of 02:25, 1 March 2017

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Introduction[edit | edit source]

Exercise training puts demands on human physiological systems, in order to maintain homeostasis.
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; acid imbalance, and by varying hormone levels.

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[1].

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)[2] 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.

References[edit | edit source]

References will automatically be added here, see adding references tutorial.

  1. Joseph T. Wearn. THE EXTENT OF THE CAPILLARY BED OF THE HEART. J Exp Med. 1928 Jan 31; 47(2): 273–290.
  2. 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.