OXYGEN DEBT THEORY AND EXCESS POST-EXCESSIVE

OXYGEN CONSUMPTION

SUBMITTED BY: Dr. Rekha G.

MSc. CND, 4th Semester
P.I.M.S., Kommaghatta,
Bengaluru.
SUBMITTED TO: Department of Sports Nutrition,
St Aloysius College ,

DATE OF SUBMISSION: 03/06/2020

 OXYGEN DEBT THEORY

Since the beginning of the 20th century physiologists have known that when an
isolated, frog muscle was stimulated to contract, lactic acid was produced as
part of the contractile response and that oxygen was necessary during
recovery to metabolize the lactic acid to eliminate its presence. These
phenomena formed the Hill-Meyerhof “Oxygen Debt” theory, which proposed
that during recovery, one-fifths of the produced lactate back to glycogen. The
findings, in part, resulted in the Nobel Prize being awarded to A.V.Hill and Otto
Meyerhof in 1922.
In year 1933, Margaria, Edwards and Dill at Harvard Fatigue Laboratory,
published their seminar Paper, which attempted to elaborate on the oxygen
debt theory by studying the oxygen consumption and blood lactate kinetics in
human subjects during and after short duration treadmill exercise of high
intensities for 4-10 minutes. Their key findings were that,
1.Recovery oxygen consumption rapidly declined initially and slowly tailed off
toward resting values, a process that took approximately one hour.
2.The high level of lactic acid that was present in the blood at the end of
exercise did not decline immediately and then it declined slowly with kinetics,
approximating the observed pattern of the oxygen consumption response.
Margaria and associates explained that the first fast phase of the post exercise
oxygen consumption curve was not temporarily associated with a change in
blood lactate. This phase was termed as “Alactacid” meaning not associated
with lactate metabolism. Also they proposed that the second, slow post
exercise oxygen consumption curve which temporarily coincided with the
decline in blood lactate, was due to the reconversion of lactate to glycogen.
Thus this slow phase was termed the “lactacid” component of the oxygen debt.
This was significant not only for defining two phases of the oxygen debt
response, but also for conceptually departing from the classical work of
Meyerhof and Hill and coworkers.
EXECESS POST- EXERCISE OXYGEN CONSUMPTION (EPEOC)

The need for oxygen to replenish ATP and remove lactic acid is referred to as
“Oxygen Debt” or “Excess Post-exercise Oxygen Consumption” (EPEOC)- the
total oxygen consumed after exercise above a pre-exercise baseline level.
During muscular exercise, blood vessel in muscles dilate and blood flow in
increased to increase the available oxygen supply. Up to a point, the available
oxygen is sufficient to meet the energy needs of the body. However, when
muscular exertion is very high, oxygen cannot be supplied to muscle fibres fast
enough, and the aerobic breakdown of pyruvic acid cannot produce all the ATP
required for further muscle contraction.
During such periods, additional ATP is generated by anaerobic glycolysis. In the
process most of the pyruvic acid produced is converted to lactic acid. About
80% of the lactic acid diffuses from the skeletal muscles and is transported to
the liver for conversion back to glucose or glycogen.
Ultimately, once adequate oxygen is available, the lactic acid must be entirely
catabolized into carbon dioxide and water. After exercise has stopped, extra
oxygen is required to metabolize lactic acid to replenish ATP, phosphocreatine
and glycogen and to pay back any oxygen that has been borrowed from
hemoglobin, myoglobin, air in the lungs and body fluids.
The additional oxygen that must be taken into the body after vigorous exercise
to restore all systems to their normal states is called Oxygen debt. Eventually
muscle glycogen must also be restored. This is accomplished through diet and
may take several days depending on the intensity of exercise. The maximum
rate of oxygen consumption during the aerobic catabolism of pyruvic acid is
called “maximal oxygen uptake”. It is determined by sex, age and size of the
body.
Highly trained athletes can have maximal oxygen uptakes that are twice tat of
average people, probably owing to a combination of genetics and training. As a
result, they are capable of higher muscular activity without increasing their
lactic acid production and their oxygen debts are less. It is for these reasons
that they do not become short of breath as readily as untrained individuals.
OXYGEN CONSUMPTION FOLLOWING EXERCISE:
After a strenuous exercise, four tasks need to be completed. They are,
1. Replenishment of ATP
2. Removal of lactic acid
3. Replenishment of myoglobin with oxygen
4. Replenishment of glycogen
In low-intensity, primarily aerobic exercise about one half of the total EPEOC
take place within 30 seconds of stopping the exercise and complete recovery
can be achieved with several minutes. Recovery from more strenuous exercise
which is often accompanied by an increase in blood lactate and body
temperature and may require 24 hours or more before re-establishing the pre-
exercise oxygen uptake. The amount of time will depend on exercise intensity
and duration.
The two significant components of oxygen recovery are:
*Alactacid oxygen debt: Is the portion of oxygen required to synthesis and
restore muscle phosphagen stores i.e. ATP
*Lactacid oxygen debt: Is the portion of oxygen required to remove lactic acid
from the muscle cells and blood.
The replenishment of muscle myoglobin with oxygen is normally completed
within the time required to recover the Alactacid oxygen debt component. The
replenishment of muscle and liver glycogen stores depends on the type of
exercise. In essence, short distance, high-intensity my take up to 2 or 3 hours
and long endurance activities may take several days. The replenishment of
glycogen stores is most rapid during the first few hours following training and
then can take several days to complete. Complete restoration of glycogen
stores is accelerated with a high carbohydrate diet.
REFERANCES
1.BANG O. The lactate contact of the blood during and after
muscular exercise in man. Skand Arch Physiol 74, Suppl 10: 49-82,
1936.
2.Brooks GA and Gaesser G. Glycogen synthesis and metabolism of
lactic acid after exercise Am J Physiol 224: 1162-1166, 1973
3.Cori CF. mammalian carbohydrate metabolism. Physiol Rev 11;
143-275,1931
4.Gladden L.B.. lactate metabolism: a new paradigm for the third
millennium J. Physiol 558: 5-30, 2004.
5.Hill .A.V and Lupton J. muscular exercise,lactic acid, and the supply
and utilization of oxygen. Q J Med 16: 135-171, 1923