What Is Oxygen Debt?

14.09.2023 Grady A. Lowry 0 Comments

Contents

0.1 What is definition of oxygen debt?
0.2 What is an oxygen debt and how is it gotten rid of?

1 What is the purpose of oxygen debt?
2 What happens when you go into oxygen debt?
3 Which best describes oxygen debt?
4 Is oxygen debt bad?
5 How can we stop oxygen debt?
- - 5.0.1 What’s the difference between oxygen debt and oxygen deficit?
6 How does oxygen debt affect the brain?
7 Why paying back oxygen debt?
8 Why is it called oxygen debt?
- - 8.0.1 Is it bad to have zero debt?
9 What is oxygen deficit versus oxygen debt?
- 9.1 Muscle Contraction, Muscle Fatigue, and Oxygen Debt | Biology and Physiology
10 What is the oxygen debt and its types?
11 What are the two types of oxygen debt?
- 11.1 What is carbon dioxide oxygen debt?

What is definition of oxygen debt?

A temporary oxygen shortage in the body tissues arising from exercise is called oxygen debt. In details, Oxygen debt is the oxygen required (after vigorous exercise, using up the oxygen faster than it can be breathed in) to oxidize lactic acid, created from anaerobic cellular respiration.

What is an oxygen debt and how is it gotten rid of?

Dictionary.com states ‘oxygen debt is the body’s oxygen deficiency resulting from strenuous physical activity.’ An oxygen debt is also described as ‘the extra oxygen that must be used in the oxidative energy processes after a period of strenuous exercise to reconvert the lactic acid build up to glucose as well as the

What is the purpose of oxygen debt?

The O2 debt was hypothesized to represent the oxidation of a minor fraction (1/5) of the lactate formed during exercise, to provide the energy to reconvert the remainder (4/5) of the lactate to glycogen during recovery.

What happens when you go into oxygen debt?

SureHire explains oxygen debt – Oxygen is used by the cells to produce energy using a process called aerobic respiration. During strenuous exercise, the body cannot deliver enough oxygen to the muscle cells. This status is referred to as an oxygen deficit.

Once the body reaches a state of oxygen deficit during exercise, energy is produced using anaerobic respiration. Anaerobic respiration breaks down glucose into energy that the cells can use to function. The process creates a waste substance called lactic acid. During aerobic respiration, this lactic acid is further broken down into carbon dioxide and water.

Oxygen is needed for this step to take place. When the body lacks the necessary oxygen to complete the process of respiration and eliminate the lactic acid, it is said to be in oxygen debt. After an individual’s activity level slows, he or she will take in extra oxygen to gradually repay this oxygen debt, allowing the cells to process the built up lactic acid.

Which best describes oxygen debt?

Now we can answer our question, which asks us to select the answer that best describes what is meant by oxygen debt. We know that the correct answer choice must be (B). An oxygen debt is the amount of oxygen required after exercise to remove the lactic acid from the body.

Is oxygen debt bad?

The Benefits of Oxygen Debt – The process of oxygen debt is not only necessary for restoring the oxygen balance in our bodies, but it also has several other benefits. During oxygen debt, your body keeps exerting itself for longer. The increased oxygen consumption helps to speed up the recovery process, reducing muscle soreness and fatigue.

How can we stop oxygen debt?

Increase in oxygen delivery by augmenting cardiac output or by increasing fraction of inspired oxygen (FiO 2 ) can help reduce oxygen debt.

What’s the difference between oxygen debt and oxygen deficit?

Study Objectives · To define factors of importance to oxygen uptake, cardiac output, and ventilation during exercise. · To describe the rise in ventilation, oxygen uptake and cardiac output during increasing exercise intensity, the concepts anaerobic threshold, oxygen deficiency and oxygen debt.

· To calculate the relationship between the major variables.
· To explain the metabolism and limits of exercise, typical sport injuries, doping, the effects of training including health consequences, and hypotheses of the cardiopulmonary regulation.
· To use the concepts in problem solving and case histories.

Principles · The human body has a redundancy of overlapping cardio-pulmonary control systems during exercise. · The redundancy-hypothesis, with neural factors dominating at the start of work and peripheral feedback control during steady state, is a possible explanation of the hyperpnoea of exercise and the related increase in cardiovascular activity,

Definitions · Anaerobic threshold.
This is the exercise level above which the energy requirements can be satisfied only by the combined aerobic metabolism and anaerobic glycolysis.
Lactic acid is produced and stimulates the peripheral chemoreceptors.
Hereby, ventilation starts to increase out of proportion to the rise in oxygen uptake.

· Blood doping. Blood boosting is an artificial improvement of performance through an increase in the haemoglobin binding capacity. Blood doping (one litre) definitely improves the oxygen transport with the blood and also the maximal oxygen uptake, which is beneficial to distance runners.

· Doping : Athletes who use drugs or other means with the intention to improve performance artificially are doped by definition. · Endurance capacity or fitness number is given as the maximal oxygen uptake in ml of oxygen STPD min -1 kg -1, · Energy equivalent of oxygen on a mixed diet is defined as the heat energy liberated in the body per litre of oxygen used (20 kJ of energy per litre at an RQ of 0.8).

· Flow Units (FU) measure relative bloodflow as the number of ml of blood passing an organ per 100 g of tissue and per min. · Mean Arterial Pressure (MAP) is the arterial blood pressure measured as the sum of the diastolic pressure plus 1/3 of the pulse pressure (see below).

· Mechanical efficiency is the ratio between external work and the total energy used during work. · Oxygen debt is defined as the extra volume of oxygen that is needed to restore all the energetic systems to their normal state after exercise. · Oxygen deficiency is defined as the difference in oxygen volume between an ideal, hypothetical oxygen uptake and the actual uptake in real life.

The missing oxygen volume at the initiation of exercise is the oxygen deficit. · Pseudo-doping. Many drugs reputedly increase athletic performance, but the fact remains that such effects rarely show up in double-blind controlled trials. – On the contrary, serious side effects occur with a biologically high and statistically significant frequency.

Essentials This paragraph deals with 1.
Athletes and training, 2.
Fitness testing, 3.
Limits of exercise performanc e, 4.
T he anaerobic threshold, 5.
Ventilation and oxygen uptake, 6.
Cardiopulmonary control, and 7.
Oxygen debt and deficiency.1.
Athletes and training At the start of exercise, signals from the brain and from the working muscles bombard the cardiopulmonary control centres in the brainstem.

Both cardiac output and ventilation increase, the a -adrenergic vasoconstrictor tone of the muscular arterioles falls abruptly, whereas the vascular resistance increases in inactive tissues. The systolic blood pressure increases, whereas the MAP only rises minimally during dynamic exercise.

The total peripheral vascular resistance ( TPVR ) falls during moderate exercise to 0.25-0.3 of the level at rest, because of the massive vasodilatation in the muscular arterioles of almost 35 kg muscle mass.
This is why the major portion of cardiac output passes through the skeletal muscles ( Fig.18-1 ) and why the diastolic pressure often decreases during exercise.

The coronary bloodflow increases, and at some intensities of exercise we see increases in the skin bloodflow (Fig.18-1). Fig.18-1 : Distribution of cardiac output during exercise. HBF means hepatic bloodflow, and CBF is cerebral bloodflow. A top athlete increases his cardiac output from 5 to 30-40 l of blood per min, when going from rest to maximal dynamic exercise (Fig.18-1).

However, the muscle bloodflow can rise 25 fold in the total muscle mass. Accordingly, the total muscular oxygen uptake rises 85 fold from rest to maximal exercise (see Table 8-1 with calculations). Training improves the capacity for oxygen transport to the muscular mitochondria, and improves their ability to use oxygen.

After long-term endurance training the athlete typically has a lower resting heart rate, a greater stroke volume, and a lower TPVR than before. The maximum oxygen uptake progressively increases with long-term training, and the extraction of oxygen from the blood is increased.

The lung diffusion capacity for oxygen probably increases by endurance training. The capillary density of skeletal muscles, the number of mitochondria, the activity of their oxidative enzymes, ATPase activity, lipase activity and myoglobin content all increase with endurance training. Endurance training also produces a rise in ventricular diastolic volume.

Strength training (weight lifting) produces a rise in left ventricular wall thickness without any important increase in volume During dynamic exercise the stroke volume increases as does heart rate, and the residual ventricular volume decreases (Fig.18-2). Fig.18-2 : The pressure-volume loop of the left ventricle in a healthy male at rest (red curve) and during dynamic exercise (blue curve). Although the peak ventricular pressure during systole rises considerably and thus the arterial peak pressure, the diastolic pressure falls because of the massive fall in total peripheral vascular resistance.

The contractility of the heart is depicted as the slope of the pressure-volume curve. The contractility increases considerably from rest to exercise (Fig.18-2).2. Fitness testing A simple objective method of estimating the endurance capacity or fitness number (maximal oxygen uptake, V ° O2 max) in a person, is to measure the heart rate (HR) at a standardised work on a cycle ergometer.

The test rests on the assumption, that there is a linear increase in HR with increasing oxygen uptake or work rate ( Fig.18-3 ). The net mechanical efficiency is relatively constant in each individual (approximately 20%). On a mixed diet the energy equivalent for oxygen is 20 kJ per l (STPD), so it is easy to calculate the volume of oxygen corresponding to any maximal work rate extrapolated from Fig.18-3. Fig.18-3 : The relationship between work intensity and steady state heart rate at work. The fitness number is in ml STPD oxygen per min and per kg of body weight. The work intensity on the ergometer is chosen to produce a heart rate between 130-150 beats per min, and must be continued for at least 5 min in order to secure respiratory steady state.

Respiratory steady state means that the pulmonary oxygen uptake is equal to the oxygen uptake of the tissues. This implies that ventilation and heart rate at work is also stable. As a standard work rate of 100 W is chosen for females, and 150 W is standard for untrained males. An optimally performed fitness test results in a heart frequency of 130-160 beats per min.

The submaximal test is designed by P.-O. Åstrand (and is sometimes performed at 2 work rates – Fig.18-3). Since the rise in HR is linearly correlated to the work rate, a line is drawn through the points (Fig.18-3). The line is extended until it reaches the horizontal line (maximal HR).

Here, the maximal heart rate is the mean of the maximal heart rate of persons of the same age and sex.
The rise in mean arterial pressure (MAP) during dynamic exercise is often minimal, because of the arteriolar dilatation with a large, rhythmic bloodflow through the working muscles.
The TPVR is typically reduced to 1/4 of the value at rest.

In contrast, static exercise often results in a doubling of the MAP, because a large muscle mass is contracting and the contraction is maintained. Static work is typically accomplished with a low cardiac output, so the TPVR is relatively high. This is dangerous to elderly people with known or unknown degrees of atherosclerosis.3.

Limits of exercise performance The limitation of performance (measured as oxygen uptake) depends upon the type of work and upon the person.
Several factors are involved.
The mass balance principle provides an overview (see Eq.18-1 ).
Both the maximum cardiac output and the maximum arterio-venous O 2 content difference are limiting factors.

Healthy persons have redundant ventilation and diffusion capacity in their lungs imposing no limitation.3.1, Pulmonary ventilation, Increasing work rate (with 15 W more each min) leads to a marked increase in pulmonary ventilation without any ceiling being reached even at maximal oxygen uptake ( V ° O2 max).

The steeper rise in ventilation is shown by its deviation relative to the thin line towards the right ( Fig.18-4),
Light exercise often increases ventilation by an increased tidal volume (V T ).
With increasing work rate also the respiratory frequency must rise from 10 towards 50 respiratory cycles per min.

The tidal volume can increase to half the value of the vital capacity (6 l), which corresponds to an exercise ventilation of (3*50=) 150 l per min. At exhaustion the ventilation is much greater than at the point, where maximal oxygen uptake is already reached.

At this maximum many individuals can increase ventilation further voluntarily.
The alveolar gas tensions, P AO2 and P ACO2, are essentially maintained during most work rates.
At maximal work rate the P AO2 increases and P ACO2 decreases 5-10%.
This fact illustrates effective gas exchange or adequate ventilation during non-exhausting exercise.

Thus ventilation is not the limiting factor in these healthy persons.3.2. The oxygen utilisation in the tissues is not a likely limitation in healthy people. A group of skiers increased their maximal oxygen uptake further, when they started arm work during continued running.

Obviously, the maximal oxygen uptake measured during running is not always maximal.3.3 Pulmonary diffusion capacity for oxygen with failure of the lungs to fully oxygenate blood.
This is certainly not a limiting factor in healthy persons with a redundant lung diffusion capacity.
The arterial blood is fully saturated with oxygen even during the most strenuous exercise at sea level.

The lung diffusion capacity (D L02 ) increases, because the number of open lung capillaries is increased, the surface area increases and the barrier-thickness is reduced. In addition, O 2 transport is boosted further by the rise in cardiac output from 5 to 30 l of blood per min Oedema or interstitial pulmonary fibrosis leads to thickening of the alveolar-capillary barrier, which will impede O 2 exchange.

The reason is that the pulmonary vascular volume is reduced (reduced capillary transit time), and thus the diffusion equilibrium point is moved towards the end of the capillary. If patients with lung diseases try to exercise, this problem is further aggravated by the still more reduced capillary transit time.

Thus exercise would impose a significant diffusion limitation on O 2 transfer.3.4. Cardiac output, Limited transport capacity for oxygen caused by limited peripheral bloodflow is the only logical explanation. Limitations in reducing TPVR or in the pumping capacity of the heart could cause the limited muscle bloodflow.

When work is maintained at peak cardiac output and maximal oxygen uptake, the blood pressure falls as more vasodilatation occurs and there are no signs of even a slight relative increase in the low TPVR,
The major limitation to exercise in well-trained athletes is the heart’s pumping capacity in delivering oxygen to the working muscles.4.

The Anaerobic threshold The anaerobic threshold (AT) is the exercise level at which the energy requirements can be satisfied only by the combined aerobic metabolism and anaerobic glycolysis. The lactic acid formed in the muscle cells diffuse into the blood and causes a metabolic acidosis, which stimulates the peripheral chemoreceptors.

Hereby, ventilation starts to increase out of proportion to the rise in oxygen uptake (Fig.18-4).
Just after the AT is passed, the ventilation increases proportional to the increase in carbon dioxide output (ie, so-called normo-capnic buffering).
Accordingly, ventilation increases linearly with carbon dioxide output but out of proportion with the oxygen uptake.

The carbon dioxide output and ventilation will increase faster than oxygen uptake, because bicarbonate react with the lactic acid produced, so CO 2 is liberated, added to the metabolic CO 2 production and eliminated by hyperventilation, causing P aCO2 to fall (ie, hyperventilation) The rise in blood is gradual, and Fig.18-4 does not show any sign of a lactic acid threshold at the anaerobic threshold. Fig.18-4 : Ventilation and arterial blood concentrations (pH, lactate and bicarbonate) at rest and during an incremental work test on a cycle ergometer up to 100%. Lactate is produced even at light exercise, but only minimal amounts are liberated to the blood (Fig.18-4).

Untrained subjects at any oxygen uptake, have higher ventilation and heart rate than the trained.
The AT in untrained persons is often about 50% of maximal oxygen uptake, whereas the AT of athletes approaches 80%.
Patients with heart disease increase their blood at a minimal activity.
The oxyhaemoglobin dissociation curve is moved progressively to the right as exercise intensity increases due to the rise in 2,3-diphosphoglycerate (DPG) concentration ( Fig.8-3 ) and to the rise in temperature.

Above the AT, when oxidative metabolism is high, extra mechanical output is financed by anaerobic energy generation. The end product is lactic acid ( Fig.18-4 ). The lactic acidosis causes a further shift to the right of the oxyhaemoglobin dissociation curve easing oxygen delivery to the mitochondria.

Lactate, nitric oxide and adenosine also dilatate muscle vessels and increase the number of open capillaries, thus improving the diffusion of oxygen from capillary blood to the mitochondria.
It is generally believed that the human brain during normal conditions combusts glucose exclusively.
This assumption has to be modified.

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The brain uptake of lactate equals that of glucose during supra-maximal work (Kojiro et al., 2000).5. Ventilation and oxygen uptake Results from an untrained person with a maximal oxygen uptake of 2.7 l STPD min -1 (AT: 1.3 l STPD min -1 ), and from a top athlete with 6 l STPD min -1 (AT: 3.6 l STPD min -1 ) are shown in Fig.18-5.

Several studies have shown oxygen uptake to remain at maximal level despite increasing work rates, and with carbon dioxide output increasing too.
These curves also illustrate that ventilation – in these persons -is not the limiting factor for maximal oxygen uptake.
If the athlete is suddenly breathing oxygen instead of atmospheric air, while working at a high level (5-6 l STPD min -1 ), a drastic fall in ventilation will occur within 30 s.

This is not a chemoreceptor response, since there is no stimulus. The oxygen breathing reduces the blood, but not within 30 s. Oxygen breathing abruptly increases the diffusion gradient and thus the rate of diffusion from haemoglobin to the muscle mitochondria. Fig.18-5 : Ventilation and oxygen uptake in an untrained person with a maximum oxygen uptake of 2.7 l per min. Results from a top athlete, with a V ° O2 max of 6 l min -1 breathing air (•) or oxygen (o) is shown for comparison. Strenuous exercise is also associated with a rise in plasma concentration of catecholamines, dehydration and a rise in core temperature approaching 41 o C.

The sensitivity of most receptors is increased in an overheated body.
Increased activity of the arterial chemoreceptors causes hyperventilation in exercise situations where plasma-K + is high and P aO2 is dangerously low.
The athlete approaches exhaustion and collapse.6.
Cardiopulmonary control The proportional increase in ventilation and cardiac output with increasing oxygen uptake suggests a common control system.

The integrator consists of sensory and motor cortical areas, and the brain stem neighbour-centres for respiratory and cardiovascular control. The link between the respiratory and the circulatory control system is probably established in the neural network of the brain stem centres.

The nucleus of the tractus solitarius is the site of central projection of both chemoreceptors and baroreceptors.
The respiratory and the cardiovascular systems are connected during most forms of dynamic exercise ( Fig.18-6 ), but they can also operate differently.
There is a sharp rise in ventilation within the first breath at the on-set of exercise, and cardiac output also increases abruptly (Fig.18-6).

Both variables increase progressively over minutes until a steady state is reached. At the offset of exercise, ventilation and cardiac output falls instantly (Fig.18-6). The cardiopulmonary adjustments to exercise comprise an integration of I. neural and II.

Humoral factors.I.
The neural factors consist of: 1) Signals from the brain, 2) Reflexes originating in the contracting muscles, and 3) the central & peripheral chemoreceptors.1.
Signals from the brain to the active muscles passes the reticular activating system (RAS) in the reticular formation of the medulla, which includes the respiratory (RC) and cardiovascular centres.

This signal transfer is called irradiation from the motor cortex to the RC, and proposed as an explanation of the exercise hyperpnoea. The mesencephalon and hypothalamus are also involved in the Krogh irradiation hypothesis now called central command. Fig.18-6 : The exercise hyperpnoea and the rise in cardiac output follow the same pattern.2 Afferent signals from proprioceptors in the active muscles through thin myelinated and unmyelinated fibres in the spinal nerves (type III and small unmyelinated type IV) to RC are the best-documented feedback hypothesis.3.

Central and peripheral chemoreceptors are sensitive to the final product of metabolism, carbon dioxide.
The carbon dioxide molecule is most likely the controlled variable, perhaps as P aCO2,
The pH, P aO2, and P aCO2 are normal during moderate steady state exercise, where the central chemoreceptors dominate.

However, during transitions from rest to exercise and during severe exercise the peripheral chemoreceptors are stimulated. Stimulation of peripheral chemoreceptors increases the rate and depth of respiration and causes vasoconstriction. II. The humoral factors that influence skeletal muscle bloodflow, cardiac output and ventilation are metabolic vasodilatators and hormones.

Neural and chemical control mechanisms oppose each other.
During muscular activity the local vasodilatators supervene.
The local vasodilatators have not been identified.
Ischaemic mitochondria in fast oxidative muscle fibres release many vasodilatators such as adenosine, AMP, and ADP.
However, it is possible to block many of the neural and humoral factors without disturbing the proportional exercise hyperpnoea and the rise in cardiac output,

These experiences suggest that the human body have a redundancy of overlapping control systems. The redundancy-hypothesis, with neural factors dominating at the start of work and peripheral feedback control during steady state, is a logical compromise.7.

Oxygen debt and deficiency The O 2 deficit is defined as the difference in O 2 volume between an ideal, hypothetical O 2 uptake and an actual uptake as it occurs in real life (see Fig.18-7 ). The missing O 2 volume is the oxygen deficit. The energy demand increases instantaneously at the start of a working period, but the actual O 2 uptake via the lung lags behind for 2 min.

The oxygen demand deficit is provided for by the O 2 stores (oxymyoglobin) and by anaerobic energy. Fig.18-7: The oxygen deficit and the oxygen debt at exercise. The oxygen debt is defined as the extra volume of O 2 that is needed to restore all the energetic systems to their normal state after exercise (Fig.18-7). The non-lactic O 2 debt following moderate work is characterised by maintained blood lactate concentration around the normal resting value of 1 mM.

The non-lactic debt is maximally 3 l, used for regeneration of the Phosphocreatine and for refilling the O 2 stores.
The lactacide O 2 debt following supramaximal work (100-400 m dash) can amount to 20 l and the blood to as high as 20-30 mM.
This O 2 debt is used for oxidation of 75% of the lactate produced, and for the formation of 25% of the lactate to glycogen in the liver.

Restoration of Phosphocreatine etc following activity, is a process referred to as repayment of the O 2 debt. However, it is very uneconomical, since the debt is often twice as high as the O 2 deficit. Pathophysiology The pathophysiology of sports is related to the ultimate limits of human performance.

Severe exercise for prolonged periods, such as a 20-fold rise in metabolic rate in a marathon runner, sometimes result in life-threatening conditions: Histotoxic hypoxia with blockage of ATP production, dehydration, hyperthermia and metabolic acidosis with a pH a below 6.9. Following a short paragraph on 1.

Muscle fatigue, two consequences of aggressive attitudes in competitions are dealt with here: 2. Sport injuries and 3. Doping, The final point is 4. Fit for life,1. Muscle fatigue Muscular contraction releases a great ionic leak (Na + -influx and a K + -outflux) through the skeletal muscle membrane, which elicits the action potential ( Fig.18-8 ).

Thus the muscle cell loses K + and gains Na + during intensive exercise.
Contraction stimulates the Na + -K + -pump acutely, and training increases its activity.
Still, at high intensity exercise the ionic leaks can exceed the capacity of the Na + -K + -pump for intracellular restoration.
During intensive exercise the Osmolarity of the contracting muscle cells increases together with the capillary hydrostatic pressure.

As a consequence, the ECV and plasma volume can fall by 20% within a few min. The plasma can rise to 8 mM due to efflux from the contracting muscle cells and from red blood cells into a reduced plasma volume. Training reduces exercise-induced hyperkalaemia.

Muscle fatigue following prolonged muscle activation increases proportional to the performance and to the loss of muscle glycogen.
The insufficient and uncoordinated muscle contractions are due to the lack of glycogen and to failing neuromuscular transmission.
Exhaustion of the stores of neurotransmitters in presynaptic terminals can occur within seconds to minutes of repetitive stimulation.

Weight lifting, football dash and 100 m dash use up the phosphagen system within seconds. Exhaustion often causes a serious drawback in the systematic practice of an athlete. The body stores are totally depleted, and deleterious consequences may occur. Fig.18-8 : Skeletal muscle cell maintaining homeostasis by the activity of Na + -K + -pumps. During exercise the striated muscle cells loose K + to the ECV and the blood. The Na + -K + -pump contains Na + -K + -ATPases, which are temporarily inefficient in maintaining homeostasis during exercise (Fig.18-8).

The rise in extracellular K + is probably related to muscular fatigue and dependent upon the maximal work capacity. Following exercise there is an extremely rapid homeostatic control in healthy well-trained persons. The activity of the Na + -K + -ATPases seems optimised in well-trained persons – not necessarily the concentration of Na + -K + -ATPases in skeletal muscle biopsies.

Even minor diseases, such as a common cold, may reduce cardiac output in an endurance athlete, thus causing muscle ischaemia during the usual practise and extreme muscle fatigue. Isolated muscular fatigue is thus due to depletion of ATP stores, whereby the actin-myosin filaments form a fixed binding and develop rigor or cramps.

Neuromuscular fatigue is probably caused by progressive depletion of acetylcholine stores during prolonged, high frequency muscular activity. Fatigue can never be fully explained by a simple rise in plasma- only. Many other signals are integrated in the CNS before a person feels fatigued. Endurance athletics in a hot and humid environment can increase the temperature of the body core to more than 41 o C.

Such a level is dangerous to the brain and CNS symptoms and signs develop severe fatigue, headache, dizziness, nausea, confusion, staggering gait, unconsciousness, and profuse sweating. When the victim suddenly faints, this is termed heat stroke, which can be fatal.2.

Sport injuries Five typical categories of sport injuries are considered here.1.
Runners are almost always damaged when working at a too high velocity or high velocity combined with turning or jumping.
The force applied to the feet of a 75 kg person while walking is around (Gravity acceleration * body weight) = (9.807 m s -2 * 75 kg) = 750 kg m s -2 or 750 Newton.

The force applied to the feet while running is 3-4 fold larger Four typical injuries of runners are shown in Fig.18-9, Fig.18-9 :Two athletes showing four frequent leg and foot injuries attended by running. The typical injuries are 1) muscle fibre lesions (myopathy with tender muscles), 2) tendosynovitis (shin splint) of the tibial posterior muscle, 3) tendinitis or rupture of the Achilles tendon, and 4) subluxation of the peroneus muscle tendon.5) Dome fractures are osteochondral fractures from the talus with pain during running.

This often occurs as a complication after a foot distortion, which does not heal.6) Stress fractures are consequences of walking long distances but are also found after distance running and basketball. These injuries occur during activities (athletes, ball players) with acceleration and deceleration by running or jumping in different directions.

Quite often, the athlete is damaged following a break in the training. Even a few days of absence are enough. The athlete starts out too rapidly in order to compensate for the break in the training schedule.2. Brain injuries (Tableing) are known from serious accidents during many types of sport – in particular Tableing.

Even the elegant Tableing legend, Muhammad Ali, was seriously injured during a long – although rather successful – carrier.
Acute brain damage or brain contusion includes deeper brain structures with neuronal damage, increased intracranial pressure and brain ischaemia ( Fig.18-10),
Head injury during Tableing can result in epidural haematoma (cranial fracture with rupture of the middle meningeal artery).

The Tableer hits the floor, is unconscious, wakes up and appears in good condition. Suddenly, he collapses again, and develops hemiplegia or die. The development of subdural haematoma is insidious venous bleeding sometimes with a latency of weeks between the head injury and the clinical phenomena ( Chapter 7 ). Fig.18-10 : Professional Tableer with typical damages from the carrier. Incomplete recovery from brain damage impairs higher cerebral function, with damages of locomotion (hemiplegia), and of psychological functions (Fig 18-10). The end result for the so-called punch-drunk Tableer is chronic traumatic encephalopathy with dementia, post-traumatic epilepsy and other neurological disorders ( Chapter 4 ).3.

Ball play damages,
Cruciate ligament lesions are common from ball play (ie, handball, football, baseball, basket and volleyball).
Basketball players often land on the toe tip from height and eventually develop exostoses.
The exostosis hallucis is called basketball toe.
The nail is tender and the exostosis has to be surgically removed.

The tibial anterior muscle originates on the tibia and passes to the navicular bone. Tendinitis in the tendon of this muscle leads to oedema, pain and crepitation. Fig.18-11 : Soccer, baseball and basketball players are shown with typical injuries from the sport. Baseball finger or mallet finger is an avulsion of an extensor tendon of the finger usually including a small flake of bone (Fig.18-11). Foot distortion (distorsio pedis) frequently includes rupture of the talofibular- calcanofibular- and bifurcate ligament or even fracture (Fig.18-11).

Orthopaedic specialists must handle Malleole and other complicated fractures. Turf toe is overextension of the basal joint of the large toe – frequently during ball play. In this case the large toe is protected with spica plast.4. Skiing injuries range from trivial to fatal. The incidence of knee sprains is high, because improvements of binding design seem to be unsuccessful.

The ski acting as a moment arm ( Fig.18-12 ) magnifies external rotation of the knee. Slalom skiing is the type of skiing with most fractures. The medial collateral ligament of the knee often ruptures. Fig.18-12 : Typical skiing and tennis injuries are shown in a male and a female. Another common ski injury is the skiers thumb, During a fall the ski pole and the wrist strap tend to concentrate forces to extend the thumb at the mid phalangeal joint until the ligaments burst.5.Tennis injuries are haematoma subungualis (tennis toe) with bleeding under the nail of the big toe.

This is a painful condition – not reserved for tennis players only. The haematoma pressure is relieved by puncture through the nail. The so-called tennis fracture is a fracture of the base of the 5.th metatarsal bone ( Fig.18-12 ) The tarsal tunnel syndrome is also frequent in tennis players with pains along the medial side of the foot and toes.

This involves the tibial posterior nerve in the channel behind the inner Malleole. Tennis elbow is a painful disease of the aponeurotic fibres through which the common extensor origin is attached to the lateral humerus epicondyle. Tennis players from the strain use the name tennis elbow (Fig.18-12); only few of the sufferers actually play tennis.

Conclusion: The demand of fast progress is linked to competitive sports.
A better strategy is to practice at a relaxed level, until stamina is developed and hard training is tolerated.
Relaxed training is often so comfortable that it becomes a lifestyle.
Tender muscles are avoided by prewarming, and a careful muscle stretch program following exercise.3.

Doping Doping derives from the word dope, which means a stimulating drug. Athletes, who use drugs or other means with the intention to improve performance artificially, are doped by definition The list of forbidden drugs counts more than 3500, and it is still growing.

How does oxygen debt affect the brain?

Oxygen deficit makes nerve cells grow Undersupply of oxygen during physical and mental activity affects the entire brain Oxygen deficit, also called hypoxia, in the brain is actually an absolute state of emergency and can permanently damage nerve cells.

Nevertheless, there is growing evidence that to a certain extent, hypoxia can also be an important signal for growth.
Together with scientists from the University Hospitals of Copenhagen and Hamburg-Eppendorf, researchers from the Max Planck Institute for Experimental Medicine in Göttingen have shown in mice that mentally and physically demanding activity triggers not only a local but also a brain-wide ‘functional hypoxia’.

Although in an attenuated form, the effects are similar to oxygen deprivation. The shortage of oxygen activates, among other things, the growth factor erythropoietin (Epo), which stimulates the formation of new synapses and nerve cells. This mechanism could explain why physical and mental training have a positive effect on mental performance into old age. Functional hypoxia in the brain: Confocal image showing cortex and hippocampus of a hypoxia reporter mouse. Note the many red-labeled hypoxic nerve cells upon motor-cognitive challenge. (green: neurons, blue: nuclei) Last year, researchers at the Max Planck Institute in Göttingen found out in experiments in with that,

This ultimately leads to the formation of new nerve cells. They observed that hypoxia activates the growth factor erythropoietin (Epo) in the brain. Although it is known primarily for its stimulating effect on red blood cells, Epo also promotes the formation of nerve cells and their networking in the brain.

In a new study, the research group examined in detail which brain regions and cell types are affected by the shortage of oxygen. To do this, they used genetically modified mice that produce a molecule throughout the brain that leads to the formation of a fluorescent dye when there is an oxygen deficit.

In order to challenge the mice both mentally and physically, the researchers let them run on specially prepared running wheels for several days.
The mice had to concentrate while running on these wheels to avoid stumbling in addition to being physically exerted.
Mice that had no access to a running wheel and mice exposed to oxygen-depleted air served as comparator groups.

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The researchers also examined the activation of genes in different brain regions and cell populations in order to find out how the brain reacts to activity-induced hypoxia.

Why paying back oxygen debt?

Anaerobic respiration occurs when there is no oxygen available and so produces an oxygen debt. This debt is equivalent to the total amount of oxygen required to oxidise the lactic acid formed from this process into carbon dioxide and water. In other words, to cancel out the debt of oxygen owed.

Is oxygen debt toxic to cells?

As oxygen debt accumulates, ongoing production of these oxidants can induce increasing and irreversible cellular damage in the form of protein nitrosylation, lipid peroxidation, and DNA damage (24).

What accumulates during oxygen debt?

Extra oxygen is required to oxidise accumulated lactic acid produced during strenuous exercise.

Why do people who train or exercise have less oxygen debt?

Oxygen – 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 (an iron-containing substance similar to hemoglobin that is found in muscle fibres), 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 (Hill 1928),
Eventually, muscle glycogen must also be restored.
This is accomplished through diet and may take several days, depending on exercise intensity.

The maximum oxygen consumption rate 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). Highly trained athletes can have maximal oxygen uptakes twice that of ordinary people, probably due to genetics and training.

What are the two types of oxygen debt?

Abstract – This paper discusses under an energetic perspective the recent and older evidence supporting the classical notion that the ‘oxygen debt’, as originally defined by Margaria et al. (1933), consists of two major components: the alactic oxygen debt, with a half-time of the order of 30 sec, and the lactic oxygen debt, with a much longer half-time, similar to that of lactic acid removal from blood after exercise (approximately 15 min).

In particular, two ensuing concepts are treated, namely (i) the energetic equivalent of blood lactate accumulation in blood, whence the notions of lactic power and lactic capacity, and (ii) the energy sources allowing contraction of the oxygen deficit at the onset of square-wave exercise.
The notion of alactic oxygen deficit is rediscussed on the basis of recent evidence in humans.

The analogies between lactate accumulation during supramaximal exercise and during exercise transients are discussed under an energetic perspective.

Why is it called oxygen debt?

Oxygen debt – When a period of exercise is over, lactic acid must be removed. The body’s tolerance of lactic acid is limited. Lactic acid is taken to the liver by the blood, and either:

oxidised to carbon dioxide and water, or
converted to glucose, then glycogen – glycogen levels in the liver and muscles can then be restored

These processes require oxygen. This is why, when the period of activity is over, a person’s breathing rate and heart rate do not return to normal straightaway. The amount of oxygen required to remove the lactic acid, and replace the body’s reserves of oxygen, is called the oxygen debt,

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Is it bad to have zero debt?

Having no debt isn’t bad for your credit as long as there is some activity on your credit reports. You can have a great score without paying a penny of interest.

What is oxygen deficit versus oxygen debt?

· To calculate the relationship between the major variables. · To explain the metabolism and limits of exercise, typical sport injuries, doping, the effects of training including health consequences, and hypotheses of the cardiopulmonary regulation. · To use the concepts in problem solving and case histories.

Definitions · Anaerobic threshold. This is the exercise level above which the energy requirements can be satisfied only by the combined aerobic metabolism and anaerobic glycolysis. Lactic acid is produced and stimulates the peripheral chemoreceptors. Hereby, ventilation starts to increase out of proportion to the rise in oxygen uptake.

Muscle Contraction, Muscle Fatigue, and Oxygen Debt | Biology and Physiology

· Doping : Athletes who use drugs or other means with the intention to improve performance artificially are doped by definition. · Endurance capacity or fitness number is given as the maximal oxygen uptake in ml of oxygen STPD min -1 kg -1, · Energy equivalent of oxygen on a mixed diet is defined as the heat energy liberated in the body per litre of oxygen used (20 kJ of energy per litre at an RQ of 0.8).

Essentials This paragraph deals with 1.
Athletes and training, 2.
Fitness testing, 3.
Limits of exercise performanc e, 4.
T he anaerobic threshold, 5.
Ventilation and oxygen uptake, 6.
Cardiopulmonary control, and 7.
Oxygen debt and deficiency.1.
Athletes and training At the start of exercise, signals from the brain and from the working muscles bombard the cardiopulmonary control centres in the brainstem.

The total peripheral vascular resistance ( TPVR ) falls during moderate exercise to 0.25-0.3 of the level at rest, because of the massive vasodilatation in the muscular arterioles of almost 35 kg muscle mass. This is why the major portion of cardiac output passes through the skeletal muscles ( Fig.18-1 ) and why the diastolic pressure often decreases during exercise.

However, the muscle bloodflow can rise 25 fold in the total muscle mass. Accordingly, the total muscular oxygen uptake rises 85 fold from rest to maximal exercise (see Table 8-1 with calculations). Training improves the capacity for oxygen transport to the muscular mitochondria, and improves their ability to use oxygen.

The lung diffusion capacity for oxygen probably increases by endurance training.
The capillary density of skeletal muscles, the number of mitochondria, the activity of their oxidative enzymes, ATPase activity, lipase activity and myoglobin content all increase with endurance training.
Endurance training also produces a rise in ventricular diastolic volume.

The contractility of the heart is depicted as the slope of the pressure-volume curve.
The contractility increases considerably from rest to exercise (Fig.18-2).2.
Fitness testing A simple objective method of estimating the endurance capacity or fitness number (maximal oxygen uptake, V ° O2 max) in a person, is to measure the heart rate (HR) at a standardised work on a cycle ergometer.

Respiratory steady state means that the pulmonary oxygen uptake is equal to the oxygen uptake of the tissues. This implies that ventilation and heart rate at work is also stable. As a standard work rate of 100 W is chosen for females, and 150 W is standard for untrained males. An optimally performed fitness test results in a heart frequency of 130-160 beats per min.

Here, the maximal heart rate is the mean of the maximal heart rate of persons of the same age and sex. The rise in mean arterial pressure (MAP) during dynamic exercise is often minimal, because of the arteriolar dilatation with a large, rhythmic bloodflow through the working muscles. The TPVR is typically reduced to 1/4 of the value at rest.

Limits of exercise performance The limitation of performance (measured as oxygen uptake) depends upon the type of work and upon the person.
Several factors are involved.
The mass balance principle provides an overview (see Eq.18-1 ).
Both the maximum cardiac output and the maximum arterio-venous O 2 content difference are limiting factors.

The steeper rise in ventilation is shown by its deviation relative to the thin line towards the right ( Fig.18-4), Light exercise often increases ventilation by an increased tidal volume (V T ). With increasing work rate also the respiratory frequency must rise from 10 towards 50 respiratory cycles per min.

At this maximum many individuals can increase ventilation further voluntarily. The alveolar gas tensions, P AO2 and P ACO2, are essentially maintained during most work rates. At maximal work rate the P AO2 increases and P ACO2 decreases 5-10%. This fact illustrates effective gas exchange or adequate ventilation during non-exhausting exercise.

Obviously, the maximal oxygen uptake measured during running is not always maximal.3.3 Pulmonary diffusion capacity for oxygen with failure of the lungs to fully oxygenate blood.
This is certainly not a limiting factor in healthy persons with a redundant lung diffusion capacity.
The arterial blood is fully saturated with oxygen even during the most strenuous exercise at sea level.

The reason is that the pulmonary vascular volume is reduced (reduced capillary transit time), and thus the diffusion equilibrium point is moved towards the end of the capillary.
If patients with lung diseases try to exercise, this problem is further aggravated by the still more reduced capillary transit time.

When work is maintained at peak cardiac output and maximal oxygen uptake, the blood pressure falls as more vasodilatation occurs and there are no signs of even a slight relative increase in the low TPVR,
The major limitation to exercise in well-trained athletes is the heart’s pumping capacity in delivering oxygen to the working muscles.4.

Hereby, ventilation starts to increase out of proportion to the rise in oxygen uptake (Fig.18-4).
Just after the AT is passed, the ventilation increases proportional to the increase in carbon dioxide output (ie, so-called normo-capnic buffering).
Accordingly, ventilation increases linearly with carbon dioxide output but out of proportion with the oxygen uptake.

Untrained subjects at any oxygen uptake, have higher ventilation and heart rate than the trained.
The AT in untrained persons is often about 50% of maximal oxygen uptake, whereas the AT of athletes approaches 80%.
Patients with heart disease increase their blood at a minimal activity.
The oxyhaemoglobin dissociation curve is moved progressively to the right as exercise intensity increases due to the rise in 2,3-diphosphoglycerate (DPG) concentration ( Fig.8-3 ) and to the rise in temperature.

Lactate, nitric oxide and adenosine also dilatate muscle vessels and increase the number of open capillaries, thus improving the diffusion of oxygen from capillary blood to the mitochondria.
It is generally believed that the human brain during normal conditions combusts glucose exclusively.
This assumption has to be modified.

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Several studies have shown oxygen uptake to remain at maximal level despite increasing work rates, and with carbon dioxide output increasing too.
These curves also illustrate that ventilation – in these persons -is not the limiting factor for maximal oxygen uptake.
If the athlete is suddenly breathing oxygen instead of atmospheric air, while working at a high level (5-6 l STPD min -1 ), a drastic fall in ventilation will occur within 30 s.

The sensitivity of most receptors is increased in an overheated body.
Increased activity of the arterial chemoreceptors causes hyperventilation in exercise situations where plasma-K + is high and P aO2 is dangerously low.
The athlete approaches exhaustion and collapse.6.
Cardiopulmonary control The proportional increase in ventilation and cardiac output with increasing oxygen uptake suggests a common control system.

The nucleus of the tractus solitarius is the site of central projection of both chemoreceptors and baroreceptors. The respiratory and the cardiovascular systems are connected during most forms of dynamic exercise ( Fig.18-6 ), but they can also operate differently. There is a sharp rise in ventilation within the first breath at the on-set of exercise, and cardiac output also increases abruptly (Fig.18-6).

Humoral factors.I.
The neural factors consist of: 1) Signals from the brain, 2) Reflexes originating in the contracting muscles, and 3) the central & peripheral chemoreceptors.1.
Signals from the brain to the active muscles passes the reticular activating system (RAS) in the reticular formation of the medulla, which includes the respiratory (RC) and cardiovascular centres.

Central and peripheral chemoreceptors are sensitive to the final product of metabolism, carbon dioxide.
The carbon dioxide molecule is most likely the controlled variable, perhaps as P aCO2,
The pH, P aO2, and P aCO2 are normal during moderate steady state exercise, where the central chemoreceptors dominate.

Neural and chemical control mechanisms oppose each other. During muscular activity the local vasodilatators supervene. The local vasodilatators have not been identified. Ischaemic mitochondria in fast oxidative muscle fibres release many vasodilatators such as adenosine, AMP, and ADP. However, it is possible to block many of the neural and humoral factors without disturbing the proportional exercise hyperpnoea and the rise in cardiac output,

Oxygen debt and deficiency The O 2 deficit is defined as the difference in O 2 volume between an ideal, hypothetical O 2 uptake and an actual uptake as it occurs in real life (see Fig.18-7 ).
The missing O 2 volume is the oxygen deficit.
The energy demand increases instantaneously at the start of a working period, but the actual O 2 uptake via the lung lags behind for 2 min.

The non-lactic debt is maximally 3 l, used for regeneration of the Phosphocreatine and for refilling the O 2 stores. The lactacide O 2 debt following supramaximal work (100-400 m dash) can amount to 20 l and the blood to as high as 20-30 mM. This O 2 debt is used for oxidation of 75% of the lactate produced, and for the formation of 25% of the lactate to glycogen in the liver.

Severe exercise for prolonged periods, such as a 20-fold rise in metabolic rate in a marathon runner, sometimes result in life-threatening conditions: Histotoxic hypoxia with blockage of ATP production, dehydration, hyperthermia and metabolic acidosis with a pH a below 6.9. Following a short paragraph on 1.

Thus the muscle cell loses K + and gains Na + during intensive exercise.
Contraction stimulates the Na + -K + -pump acutely, and training increases its activity.
Still, at high intensity exercise the ionic leaks can exceed the capacity of the Na + -K + -pump for intracellular restoration.
During intensive exercise the Osmolarity of the contracting muscle cells increases together with the capillary hydrostatic pressure.

Muscle fatigue following prolonged muscle activation increases proportional to the performance and to the loss of muscle glycogen.
The insufficient and uncoordinated muscle contractions are due to the lack of glycogen and to failing neuromuscular transmission.
Exhaustion of the stores of neurotransmitters in presynaptic terminals can occur within seconds to minutes of repetitive stimulation.

The rise in extracellular K + is probably related to muscular fatigue and dependent upon the maximal work capacity.
Following exercise there is an extremely rapid homeostatic control in healthy well-trained persons.
The activity of the Na + -K + -ATPases seems optimised in well-trained persons – not necessarily the concentration of Na + -K + -ATPases in skeletal muscle biopsies.

Neuromuscular fatigue is probably caused by progressive depletion of acetylcholine stores during prolonged, high frequency muscular activity.
Fatigue can never be fully explained by a simple rise in plasma- only.
Many other signals are integrated in the CNS before a person feels fatigued.
Endurance athletics in a hot and humid environment can increase the temperature of the body core to more than 41 o C.

Sport injuries Five typical categories of sport injuries are considered here.1.
Runners are almost always damaged when working at a too high velocity or high velocity combined with turning or jumping.
The force applied to the feet of a 75 kg person while walking is around (Gravity acceleration * body weight) = (9.807 m s -2 * 75 kg) = 750 kg m s -2 or 750 Newton.

This often occurs as a complication after a foot distortion, which does not heal.6) Stress fractures are consequences of walking long distances but are also found after distance running and basketball. These injuries occur during activities (athletes, ball players) with acceleration and deceleration by running or jumping in different directions.

Even the elegant Tableing legend, Muhammad Ali, was seriously injured during a long – although rather successful – carrier.
Acute brain damage or brain contusion includes deeper brain structures with neuronal damage, increased intracranial pressure and brain ischaemia ( Fig.18-10),
Head injury during Tableing can result in epidural haematoma (cranial fracture with rupture of the middle meningeal artery).

Ball play damages,
Cruciate ligament lesions are common from ball play (ie, handball, football, baseball, basket and volleyball).
Basketball players often land on the toe tip from height and eventually develop exostoses.
The exostosis hallucis is called basketball toe.
The nail is tender and the exostosis has to be surgically removed.

Orthopaedic specialists must handle Malleole and other complicated fractures. Turf toe is overextension of the basal joint of the large toe – frequently during ball play. In this case the large toe is protected with spica plast.4. Skiing injuries range from trivial to fatal. The incidence of knee sprains is high, because improvements of binding design seem to be unsuccessful.

This is a painful condition – not reserved for tennis players only. The haematoma pressure is relieved by puncture through the nail. The so-called tennis fracture is a fracture of the base of the 5.th metatarsal bone ( Fig.18-12 ) The tarsal tunnel syndrome is also frequent in tennis players with pains along the medial side of the foot and toes.

Conclusion: The demand of fast progress is linked to competitive sports.
A better strategy is to practice at a relaxed level, until stamina is developed and hard training is tolerated.
Relaxed training is often so comfortable that it becomes a lifestyle.
Tender muscles are avoided by prewarming, and a careful muscle stretch program following exercise.3.

What is the oxygen debt and its types?

Quick Check –

EPOC is the repaying of energy after anaerobic exercise
There are two components of oxygen debt. Alactic and Lactacid.
Alactic replenishes the CP stores (takes approx 4 mins to replenish 97% of the CP)
Lactacid primarily replenishes the stored glycogen and removes lactic acid
Higher levels of aerobic fitness can result in quicker repayment of oxygen debt
There are a number of methods to speed up the recovery process including: – cool down, ice baths, correct nutrition and hydration, compression clothing and massage.

What are the two types of oxygen debt?

In particular, two ensuing concepts are treated, namely (i) the energetic equivalent of blood lactate accumulation in blood, whence the notions of lactic power and lactic capacity, and (ii) the energy sources allowing contraction of the oxygen deficit at the onset of square-wave exercise. The notion of alactic oxygen deficit is rediscussed on the basis of recent evidence in humans.

The analogies between lactate accumulation during supramaximal exercise and during exercise transients are discussed under an energetic perspective.

What is carbon dioxide oxygen debt?

This is called an oxygen debt. It is repaid after exercise. The oxygen reacts with the lactic acid to form CO2 and water. Rapid and deep breathing is needed for a short period after high intensity exercise in order to repay the debt.

Grady A. Lowry