The Recovery Process Excess Post Exercise Oxygen Consumption(EPOC): This is the excess oxygen...

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The Recovery Process Excess Post Exercise Oxygen Consumption(EPOC): This is the excess oxygen consumed following exercise which is needed to replace ATP which has been used up and to remove lactic acid created during the previous exercise. Oxygen deficit Alactic component Lactacid component EPOC VO2 . Resting o2 consumptio n

Transcript of The Recovery Process Excess Post Exercise Oxygen Consumption(EPOC): This is the excess oxygen...

The Recovery Process

Excess Post Exercise Oxygen Consumption(EPOC): This is the excess oxygen consumed following exercise which is needed to replace ATP which has been used up and to remove lactic acid created during the previous exercise.

Oxygen deficit

Alactic component

Lactacid component

EPOC

VO2

.

Resting o2 consumption

The aim of the recovery process is to :

Replace ATP/PC stores,

Remove Lactic Acid,

Replenish the myoglobin O2 stores and

Replace Glycogen.

Note : Oxygen deficit is the difference between the O2 required during the exercise and the O2 actually consumed during the activity.

The first three require O2 in substantial quantities, hence the need for rapid breathing and heart rate to carry O2 to the muscle cells. This need for O2 to rapidly replace ATP and remove lactic acid is known as EPOC.

The fourth item, glycogen replacement, is a long term process which can take 24 – 48 hours depending on the fitness level, diet of the sportsperson and the intensity and duration of the exercise.

There are many other processes involved in recovery. Processes such as restoration of cardiac/pulmonary functioning to resting values, return to normal body temperature etc. all require additional O2 ( although substantially less than that used during the alactacid and lactacid components) and therefore adds time to paying back the O2 deficit to reach the pre exercise level.

The Alactacid oxygen debt component

Both processes occur initially, though the Alactacid process is more rapid and is completed more quickly. Here O2 is used to synthesise and restore muscle phosphagen stores (ATP/PC) which have been almost completely exhausted during high intensity exercise.

120s

ATP/PC

Time

The phosphagen restoration is achieved by three mechanisms:

1. The aerobic conversion of carbohydrates into CO2 and water which is used to manufacture ATP from ADP andPi.

2. Some of the ATP is immediately used to create PC using the “coupled reaction”.

3. A small amount of ATP is remanufactured via glycogen producing small amounts of lactic acid.

The size of the alactacid debt is within a range of 1-4 litres, depending on the intensity of the exercise and the fitness of the sportsperson.

Implications for interval training:

Short interval between bouts of exercise does not allow full recovery (overload).

Level of phosphagen stores reduces as session continues.

Effects of training on the Alactacid Component

Increased stores of ATP and PC in muscle cells.

Improved ability to provide O2.

Increase in size of alactic component.

Part of the recovery mechanism following anaerobic exercise involves the replenishment of myoglobin with O2.

Myoglobin has an important , if small scale, role in carrying O2 from haemoglobin to the mitochondria thus ensuring the provision of energy in muscles.

Complete restoration is thought to be complete by the time needed to recover the alactacid debt component.

The Lactacid oxygen debt component

This slow component of recovery represents the amount of O2 consumed in order to remove accumulated lactic acid from muscle cells and blood.

Recovery time1hr

O2 debt

100%

The speed of lactate removal depends on the severity of the exercise and whether the athlete rests during recovery (known as passive recovery) or performs light exercise (known as active recovery).

This process begins as soon as lactic acid begins to appear in muscle. The lactic acid produced quickly dissociates into hydrogen ions (H+) and lactate. The lactate is a component of a salt formed when it combines with sodium (Na+) or potassium (K+) ions.

This process continues until recovery is complete.

The Effect of Lactic Acid Accumulation

During high intensity exercise, muscle fatigue occurs at a pH of 6.4 and noticeably affects muscle function. It is thought that protons dissociate from lactic acid and associate with glycolytic enzymes, thus making them acidic.

In this state, the enzymes lose their catalytic ability and energy production through glycolysis ceases. This coupled with the inhibition of the transmission of neural impulses impairs muscle contraction.

Fate of the Lactic Acid

65% is oxidised to form carbon dioxide and water.

20% is converted back into glucose by the liver (gluconeogenesis). This is returned to the liver and muscles to be stored as glycogen.

10% is converted in the liver to form protein.

5% is converted into glucose.

Soda Loading

Removal of lactic acid relies on the buffering capacity of the body, which weakens the effect of lactic acid.The blood is fairly efficient at this due to the hydrogen carbonate ion produced by the kidneys which absorbs the lactate and forms carbonic acid, which is eventually degraded to form CO2 and water, both of which are eliminated via the lungs.

Some athletes seek to improve their buffering capacity by”soda loading” which involves drinking sodium bicarbonate several minutes before an event. While performance may improve, side effects include vomiting and diarrhoea.

Measurement of Lactic Acid

Lactic acid and lactate, usually used interchangeably are not actually the same substance:

Lactate is a product of lactic acid which splits to give lactate and hydrogen ions. It is far easier to measure blood lactate levels than perform muscle biopsies!

Reasons for measuring lactate:

To determine and assess training intensities to ensure the athlete is working at a suitable level and is producing energy by the most effective energy system for their activity.

Provides data on athlete’s current work capacity and fitness levels.

Assess the effectiveness of the current training regime.

Establishes an athletes anaerobic threshold or point of ‘Onset Blood Lactate Accumulation’.

OBLA

The normal amount of lactate circulating in the blood is about 1 – 2 millimoles of lactate per litre of blood.

In aerobic exercise this remains about the same.

In medium intensity workouts (30 min run), this amount doubles to 4 m.moles per litre. This represents the anaerobic or lactate threshold. Researchers have used this as a standard point of reference, known as the Onset of Blood Lactate Accumulation (OBLA).

In untrained people the lactate threshold occurs at around 50 – 60% of their VO2max, whereas elite endurance athletes may not reach their lactate threshold until around 70 – 80% of their VO2max.

During a high intensity training, such as a 300 metre flat-out run, lactate levels can reach up to 15 – 20 times resting values.

Most research into the speed of lactate removal suggest that 50% of the debt is repaid in the first 15 minutes after exercise and that at least one hour is required for full recovery depending on the intensity of the exercise and the fitness of the performer.

Active recovery between exercise repetitions and at the end of a session speeds up the removal of lactate.

% lactacid debt repaid 100%

Exercise recovery

50%

30 60 90 120 Time (mins)

Repayment of the lactacid oxygen debt during rest recovery and exercise recovery

  

Restoration of Muscle Glycogen Stores Following a Marathon

Full

Muscle glycogen stores

Exercise Recovery Time(hours)

Restoration of Muscle Glycogen Stores

Short duration high intensity exercise (800m) restoration up to 2 hours.

Prolonged low intensity aerobic exercise (marathon) restoration can take days.

High carbohydrate diet speeds up this process.

Fast twitch fibres restore muscle glycogen quicker than slow twitch fibres.

Need for athlete to fully restore as soon as possible after activity (high CHO loaded drinks immediately following exercise).

Muscle Soreness

Muscle soreness is often experienced during the latter stages of an exercise period, the following day after strenuous exercise or at both times. Possible explanations are the muscle spasm theory, the lactate theory and the damaged muscle and connective tissue theory.

Muscle spasms are the result of sudden involuntary muscle twitches, causing local muscle tearing which generates an inflammatory response.

The lowering of the blood’s pH during intense exercise is sensed by pain receptors. Active recovery allows active muscle to be flushed with oxygenated blood reducing the effects of lactate and speeding up recovery.

Muscle soreness felt the day after strenuous exercise , DOMS (Delayed Onset Muscle Soreness), may be caused through injury to muscle and connective tissue. Excessive mechanical forces (often eccentric in nature) cause structural damage.Muscle protein breakdown causes inflammation or tissue oedema which stimulate local pain receptors.