From: http://www.zuniv.net/physiology/book/chapter18.html 1. The human body has a redundancy of overlapping cardio-pulmonary control systems during exercise. 2.

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 min1 kg-1. (Standard Air Temperature and Air Pressure Dry) 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. 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. 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). 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 -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 and why the diastolic pressure often decreases during exercise. The coronary blood flow increases, and at some intensities of exercise we see increases in the skin blood flow (Fig. 18-1).

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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. 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).

The pressure-volume loop of the left ventricle in a healthy male at rest (red curve) and during dynamic exercise (blue curve).
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A simple objective method of estimating the endurance capacity or fitness number (maximal oxygen uptake, VO2max) 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. 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 calcu late 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 im plies that ventilation and heart rate at work is also stable 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 out put (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 CO2 production and eliminated by hyperventilation, causing PaCO2 to fall (ie, hyperventilation). The rise in blood [lactate] is gradual, and does not show any sign of a lactic acid threshold at the anaerobic threshold. Note the total rise in plasma [lactate] of 10 mM, which is equal to the fall in plasma [bicarbonate] from 24 to 14 mM (Fig. 18-4). Exercise levels above the maximal aerobic capacity is called supra-maximal work. Here, the anoxia leading to a metabolic or lactic acidosis contribute with a large ventilatory drive, as shown in the steep com3/6

ponent of VE (Fig. 18-4 and 18-5).

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%.

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 O2max of 6 l min-1 breathing air () or oxygen (o) is shown for comparison. Lactate is produced even at light exercise, but only minimal amounts are liberated to the blood (Fig. 184). 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 [lactate] at a minimal activity. Above the AT, when oxidative metabolism is high, extra mechanical output is financed by anaerobic en ergy 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,
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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. The brain uptake of lactate equals that of glucose during supramaximal 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 at mospheric 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 [lactate], but not within 30 s. Oxygen breathing abruptly increases the diffusion gradient and thus the rate of diffusion from haemoglobin to the muscle mitochondria. Exhaustive exercise with a severe metabolic acidosis may cause the steep rise in ventilation without a further rise in oxygen uptake (Fig. 18-5). In this case, oxygen seems to diffuse at a reduced rate 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 VO2max 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 PaO2 is dangerously low. The athlete approaches exhaustion and collapse.

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6. Oxygen debt and deficiency The O2 deficit is defined as the difference in O2 volume between an ideal, hypothetical O2 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 O2 debt following supramaximal work (100-400 m dash) can amount to 20 l and the blood [lactate] 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 O2 deficit.

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