Transcript A level Recovery Processes - rcs-pe

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.
.
VO2
Oxygen deficit
Alactic component
Lactacid
component
Resting o2
consumption
EPOC
Note : Oxygen deficit is the difference between
the O2 required during the exercise and the O2
actually consumed during the activity.
The aim of the recovery process is to :
Replace ATP/PC stores,
Remove Lactic Acid,
Replenish the myoglobin O2 stores and
Replace Glycogen.
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.
ATP/PC
120s
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.
O2 debt
100%
1hr
Recovery time
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.