Muscle fatigue and Oxygen Debt

1. MUSCLE
FATIGUE AND
OXYGEN DEBT
200LEVEL RS PROGRAMME
DR A.Z. LAWAL
DEPARTMENT OF MEDICAL BIOCHEMISTRY,
UNIVERSITY OF LORIN.

2. Objectives
 Definition of terms
 Overview of energy metabolisms
 Oxygen Debt and it’s mechanism
 Importance of oxygen debt
 Components of oxygen recovery
 Muscle fatigue and it’s mechanism
 Effect of muscle fatigue on performance

3. DEFINITION OF TERMS
 Muscle fatigue: ↓ ability of muscles to
contract, or generating
 Exhaustion: required force or exercise
intensity can no longer be maintained
 Weakness - lack of physical or muscle
strength
 Oxygen debt: extra oxygen required by
muscle tissue

4. Definition of terms cont.
 ATP: multifunctional nucleoside triphosphate
used in cells as a coenzyme (molecular unit of
currency" of intracellular energy transfer)
 Creatine phosphate: phosphorylated creatine
molecule
 Lactic acid (milk acid): chemical compound
that plays a role in various biochemical
processes

5. ‘

7. Glucose-alanine cycle
Alanine brings both carbon
and nitrogen from muscle
to liver.
7

8. The mechanisms allow muscle cells
to produce ATP with high rates at
the expense of regenerating
glucose from lactate and alanine in
the liver
What is a common feature for Cori cylcle
and Glc-Ala Cycle ?
8

9. OXYGEN DEBT
 First coined by Archibald Vivian Hill in 1922.
 A.V Hill et al, discussed energy metabolism
during exercise and recovery in Financial-
Accounting terms
 The greater the energy ‘deficit’ or use of
available energy stored credits, the larger the
energy ‘debt’ incurred.
 The recovery oxygen uptake was thought to
represent the metabolic cost of paying this debt-
hence the term Oxygen debt

10.  In more concrete terms, the accumulation of
lactic acid during the anaerobic component
of exercise represented the utilization of the
stored energy credit, glycogen.

11. The ensuing oxygen debt was believed to
serve two purposes;
 to re-establish the original carbohydrate stores
(credits) by resynthesizing approximately
80% of the lactic acid back to glycogen in the
liver and
 to catabolize the remaining lactic acid
through pyruvic acid-krebs cycle pathway and
Cori cycle in the liver

12. Mechanism Of Oxygen Debt
 During muscular exercise, blood vessels in
muscles dilate and blood flow is increased in
order to increase the 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 great,
oxygen cannot be supplied to muscle fibers fast
enough, and the aerobic breakdown of pyruvic
acid cannot produce all the ATP required for
further muscle contraction

13. Mechanism Of Oxygen Debt
cont.
 During such periods, additional ATP is
generated by anaerobic glycolysis
 Most of the pyruvic acid produced is converted
to lactic acid
 Although about 80% of the lactic acid diffuses
from the skeletal muscles and is transported to
the liver for conversion back to glucose or
glycogen

14. Mechanism Of Oxygen Debt
cont.
 Ultimately, once adequate oxygen is available,
lactic acid must be catabolized completely into
carbon dioxide and water
 After exercise has stopped, extra oxygen is
required to metabolize lactic acid to replenish;
 ATP,
 Phosphocreatine,
 Glycogen

15.  to pay back any oxygen that has been
borrowed from hemoglobin, myoglobin (an
iron-containing substance found in muscle
fibers similar to hemoglobin
 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

16.  Restoration of muscle glycogen:
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 (higher in males), age
(highest at about age 20) and size (increases
with body size).

17.  Highly trained athletes can have maximal
oxygen uptakes that are twice that of average
people, probably owing to a combination of
genetics and training
 As a result, they are capable of greater 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

18. Oxygen consumption
following exercise
After a strenuous exercise there are four tasks
needs to be completed:
 Replenishment of ATP
 Removal of lactic acid
 Replenishment of myoglobin with oxygen
 Replenishment of glycogen

19. EPOC
 "Excess Post-exercise Oxygen Consumption"
(EPOC) - the total oxygen consumed after
exercise in excess of a pre-exercise baseline
level.
 In low intensity, primarily aerobic exercise,
about one half of the total EPOC takes place
within 30 seconds of stopping the exercise and
complete recovery can be achieved within
several minutes (oxygen uptake returns to the
pre-exercise level)

20. Recovery
 Recovery from more strenuous exercise, which
is often accompanied by increase in blood lactate
and body temperature, may require 24 hours or
more before re-establishing the pre-exercise
oxygen uptake
 The amount of time will depend on the exercise
intensity and duration.

21. COMPONENT OF OXYGEN
RECOVERY
 two major components :
 Alactic acid oxygen debit (fast
component), the portion of oxygen
required to synthesise and restore
muscle phosphagen stores (ATP and
PC)
 Lactic acid oxygen debit (slow
component)

22. 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 debit
component.

23.  The replenishment of muscle and liver
glycogen stores depends on the type of
exercise:
 short distance, high intensity exercise
(e.g. 800 metres) may take up to 2 or 3
hours and
 long endurance activities (e.g.
marathon) may take several days

24.  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

25. Muscle fatigue
 Muscle fatigue, or physical fatigue, is
the decline in ability of a muscle to
generate force (ATP)
 It can be a result of vigorous exercise
but abnormal fatigue may be caused
by barriers to or interference with the
different stages of muscle contraction

26. Causes
There two main causes of muscle fatigue;
 Neural fatigue (limitation of a nerve’s
ability to generate a sustained signal)
 Metabolic fatigue ( decrease in
necessary substrates or the
accumulation of metabolites).

27. Metabolic fatigue
 Metabolic fatigue is a common term for the
reduction in contractile force due to the direct or
indirect effects of two main factors:
 Shortage of fuel (Substrates) within the muscle
fibre
 Accumulation of substances (Metabolites)
within the muscle fiber, which interfere either
with the release of calcium (Ca2+) or with the
ability of calcium to stimulate muscle
contraction.

28. Substrates
 Substrate within the muscle generally serve to
power muscular contractions
They include molecules such as
 ATP
 Glycogen
 Creatine phosphate

29.  ATP binds to the myosin head and causes the
‘ratchetting’ that results in contraction according
to the sliding filament model
 Creatine phosphate stores energy so ATP can be
rapidly regenerated within the muscle cells from
ADP and inorganic phosphate ions, allowing for
sustained powerful contractions that last between
5–7 seconds.

30.  Glycogen is the intramuscular storage
form of glucose, used to generate
energy quickly once intramuscular
creatine stores are exhausted, producing
lactic acid as a metabolic byproduct.

31. Substrates cont.
 Substrate shortage is one of the causes of
metabolic fatigue.
 Substrates are depleted during exercise,
resulting in a lack of intracellular energy
sources to fuel contractions
 In essence, the muscle stops contracting
because it lacks the energy to do so.

32. Metabolites accumulation
 Metabolites are the substances (generally waste
products) produced as a result of muscular
contraction.
 They include chloride, potassium, lactic acid,
ADP, magnesium (Mg2+), reactive oxygen
species, and inorganic phosphate.

33.  Accumulation of metabolites can directly or
indirectly produce metabolic fatigue within
muscle fibers through interference with the
release of calcium (Ca2+) from the
sarcoplasmic reticulum or reduction of the
sensitivity of contractile molecules actin
and myosin to calcium.

34. Chloride
 Intracellular chloride partially inhibits the
contraction of muscles
 It prevents muscles from contracting due to
"false alarms", small stimuli which may cause
them to contract
 This natural brake helps muscles respond
solely to the conscious control or spinal
reflexes but also has the effect of reducing the
force of conscious contractions

35. Potassium
 High concentrations of potassium (K+) also
causes the muscle cells to decrease in
efficiency, causing cramping and fatigue
 Potassium builds up in the t-tube system and
around the muscle fiber as a result of action
potentials
 The shift in K+ changes the membrane
potential around the muscle fiber

36.  The change in membrane potential
causes a decrease in the release of
calcium (Ca2+) from the sarcoplasmic
reticulum

37. Lactic acid
 It was once believed that lactic acid build-up
was the cause of muscle fatigue
 The assumption was lactic acid had a
"pickling" effect on muscles, inhibiting their
ability to contract
 The impact of lactic acid on performance is
now uncertain, it may assist or hinder muscle
fatigue

38.  Produced as a by-product of fermentation,
lactic acid can increase intracellular acidity of
muscles
 This can lower the sensitivity of contractile
apparatus to Ca2+ but also has the effect of
increasing cytoplasmic Ca2+ concentration
through an inhibition of the chemical pump
that actively transports calcium out of the cell
 This counters inhibiting effects of potassium
on muscular action potentials

39.  Lactic acid also has a negating effect on the
chloride ions in the muscles, reducing their
inhibition of contraction and leaving potassium
ions as the only restricting influence on muscle
contractions, though the effects of potassium are
much less than if there were no lactic acid to
remove the chloride ions.
 Ultimately, it is uncertain if lactic acid reduces
fatigue through increased intracellular calcium
or increases fatigue through reduced sensitivity
of contractile proteins to Ca2+

40. Nervous fatigue
 Nerves are responsible for controlling the
contraction of muscles, determining ;
 the number,
 the sequence
 and force of muscular contraction.


41.  For extremely powerful contractions that are
close to the upper limit of a muscle's ability to
generate force, nervous fatigue can be a limiting
factor in untrained individuals
 In novice strength trainers, the muscle's ability
to generate force is most strongly limited by
nerve’s ability to sustain a high-frequency
signal.

42. Effect on performance
 Fatigue has been found to play a big role in
limiting performance in sport specific skills as
follow;
 Reduced voluntary force production in fatigued
muscles (measured with concentric, eccentric,
and isometric contractions),
 Reduced throwing velocities,
 Reduced kicking power and velocity,


43.  Less accuracy in throwing and
shooting activities, endurance
capacity, anaerobic capacity,
anaerobic power, mental
concentration, and many other
performance parameters

44. Thanks for
listening!!!