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14. 7. 2012.

Physiological responses to acute altitude exposure

Respiratory responses to acute exercise

Adequate oxygen supply to exercising muscles is essential to physical performance and it depends on an adequate supply of oxygen being brought into the body, moved  from the lungs to the blood, transported to the muscles, and adequately taken up into the muscles. A limitation in any of these steps can impair performance.

The transport of oxygen to working muscle begins with pulmonary ventilation, the active transport of gas molecules into the alveoli of the lungs(breathing). Ventilation increases within seconds of exposure to high altitude, both at rest and during exercise, because chemoreceptors in the aortic arch and carotid arteries are stimulated by the low PO2 and signals are sent to the brain to increase breathing. The increased ventilation is primarily associated with an increased tidal volume, although respiratory rate also increases. Over the next several hours and days, ventilation remains elevated to a level proportional to the altitude.
Increased ventilation acts much the same as hyperventilation at sea level. The amount of carbon dioxide in the alveoli is reduced. Carbon dioxide follows the presture gradient, so more diffuses out of the blood, where its pressure is relatively high, and into the lungs to be exhaled. This “blowing off” of CO2 causes blood PCO2 to fall and blood pH to increase, a condition known as respiratory alkalosis. This alkalosis has two effects. First, it causes the oxyhemoglobin saturation curve to shift to the left. Second, it helps limit the rise in ventilation but is overridden by the hypoxic(low PO2) drive. At a given submaximal exercise intensity, ventilation is higher at altitude than at sea level, but maximal exercise ventilation is similar.
In an effort to offset respiratory alkalosis, the kidneys excrete more bicarbonate ion, the ions that buffer the carbonic acid formed from carbon dioxide. Thus, a reduction in bicarbonate ion concentration reduces the blood’s buffering capacity. More acid remains in the blood, and the alkalosis is offset.

Under resting conditions, pulmonary diffusion(diffusion of O2 from the alveoli to the arterial blood) does not limit the exchange of gases between the alveoli and the blood. If gas exchange were limited or impaired, less oxygen would enter the blood, so the arterial PO2 would be much lower than the alveolar PO2. Instead, these two values are almost equal(see picture below). Therefore, the low arterial blood PO2, or hypoxemia, is a direct reflection of the low alveolar PO2, and not an oxygen diffusion limitation from the lungs to the blood.

Oxygen transport

As shown in the figure above, the PO2 at sea level is 159mmHg; however, it decreases to  about 104 in the alveoli primarily because of the addition of water vapor molecules(PH2O = 47mmHg at 37°C). When the alveolar PO2 drops at altitude, less hemoglobin in the blood perfusing the lungs becomes saturated with O2. As depicted in the figure below, the oxygen-binding curve for hemoglobin has a distinct S shape. At sea level, when alveolar PO2 is about 104mmHg, 96% to 97% of hemoglobin has O2 bound to it. When PO2 in the lungs is decreased to 46mmHg at 4,300m(14,108ft), only about 80% of hemoglobin sites are saturated with O2. If the oxygen-loading portion of the curve were not relatively flat, far less O2 would be taken up by the blood as it passes through the lungs. Therefore, while arterial blood is still desaturated at altitude, the features of the oxyhemoglobin dissociation curve serve to minimize this problem.
A second adaptation occurs very early in altitude exposure that also aids in preventing the fall in arterial oxygen content. As mentioned earlier, a respiratory alkalosis accompanies the increased ventilation caused by acute altitude exposure. This increase in blood pH actually shifts the oxyhemoglobin dissociation curve leftward, as shown in the figure below. The result is that, rather than 80% binding of oxygen to hemoglobin, 89% of Hb is saturated with O2.

Gas exchange in the muscles

First figure shows that arterial PO2 at sea level is about 100mmHg, and the PO2 in body tissues is consistently about 40mmHg at rest; so the difference, or the pressure gradient, between the arterial PO2 and the tissue PO2 at sea level is about 60mmHg. However, when one moves to an elevation of 4,300m(14,108ft), arterial PO2 decreases to about 42mmHg, whereas the tissue PO2 drops to 27mmHg. Thus, the pressure gradient decreases from 60mmHg at sea level to only 15mmHg at the higher altitude. This represents a 75% reduction in the diffusion gradient! Because the diffusion gradient is responsible for driving the oxygen from the hemoglobin in the blood into the tissues, this change in arterial PO2 at altitude is a much greater consideration for exercise performance than the small reduction in hemoglobin saturation that occurs in the lungs.

Cardiovascular responses to altitude

As the respiratory system becomes increasingly limiting as altitude increases, the cardiovascular system likewise undergoes substantial changes to compensate for the decrease in PO2 that accompanies increased altitude.

Blood volume

Within the first few hours of arrival at altitude, a person’s plasma volume begins to progressively decrease, and it plateaus by the end of the first few weeks. This decrease in plasma volume is the result of both respiratory water loss and increased urine production. This combination of respiratory water loss and the excretion of fluid can reduce total plasma volume by up to 25%. Initially, the result of the plasma loss is an increase in the concentration of red blood cells(containing hemoglobin), allowing more oxygen to be delivered to the muscles for a given cardiac output. Because this reduction in plasma volume occurs with little or no change in the total red blood cell count, it results in a higher hematocrit but a smaller total blood volume than at lower altitudes. This diminished plasma volume eventually returns to normal if adequate fluids are ingested.
Continued exposure to high altitude triggers the release of erythropoetin(EPO) from the kidneys, the hormone responsible for stimulating erythrocyte(red blood cell) production. This increases the total number of red blood cells. These adaptations ultimately result in a greater total blood volume, which allows the person to partially compensate for the lower PO2 experienced at altitude. However, this compensation is slow, taking weeks to months to fully restore red cell mass.

Cardiac output

The preceding discussion clearly illustrates that the amount of oxygen delivered to the muscles by a given volume of blood is limited at altitude because of the reduced PO2. A logical means to compensate for this is to increase the volume of blood delivered to the active muscles. At rest and during submaximal exercise, this is accomplished by increasing cardiac output. Upon ascent to altitude, the sympathetic nervous system is stimulated, releasing norepinephrine and epinephrine, the main hormones that alter cardiac function. The increase in norepinephrine in particular persists for several days of acute altitude exposure.
When submaximal exercise is performed during the first few hours at altitude, stroke volume is decreased compared to sea-level values(attributable to the reduced plasma volume). Fortunately, heart rate is increased disproportionately to not only compensate for the decrease in stroke volume but to actually slightly increase cardiac output. However, this extra cardiac workload is not an efficient way to ensure sufficient oxygen delivery to the body’s active tissues for prolonged periods. Consequently, after a few days at altitude, the muscles begin extracting more oxygen from the blood(increasing the arterial-venous oxygen difference), which reduces the demand for increased cardiac output, since VO2 = Q x (a-ṽ)O2 difference. The increase in heart rate and cardiac output peaks after about 6 to 10 days at high altitude, after which cardiac output and heart rate during a given exercise bout start to decrease.
At maximal or exhaustive work levels at higher altitudes, both maximal stroke volume and maximal heart rate are decreased. The decrease in stroke volume is directly related to the decrease in plasma volume. Maximal heart rate may be somewhat lower at high altitude as a consequence of a decrease in the response to sympathetic nervous system activity, possibly attributable to a reduction in ß-receptors(receptors in the heart that respond to sympathetic nerve activation, thus increasing the heart rate). The effect of these changes in maximal heart rate and stroke volume is obvious: maximal cardiac output decreases. With a decreased diffusion gradient to push oxygen from the blood into the muscles, coupled with this reduction in maximal cardiac output, it is apparent why both VO2max and submaximal aerobic performance are hindered at altitude. In summary, hypobaric conditions significantly limit oxygen delivery to the muscles, reducing the capacity to perform high-intensity or prolonged aerobic activities.

Metabolic responses to altitude

Ascent to altitude increases the basal metabolic rate, possibly due to increases in either or both thyroxin and the catecholamines. This increased metabolism must be balanced by an increased food intake to prevent body weight from decreasing, a common occurrence during the first few days at altitude because appetite declines as well. In individuals who maintain their body weight at altitude, there is an increased reliance on carbohydrate for fuel, both at rest and during submaximal exercise. Because glucose yields more energy than fats or proteins per liter of oxygen, this adaptation would be beneficial.
Given the hypoxic conditions at altitude, and because any fixed amount of work at altitude represents a higher percentage of VO2max, we would expect anaerobic metabolism to be increased. If this occurs, we would expect lactic acid production to increase at any given work rate above lactate threshold. This is in fact the case upon arrival at altitude. However, with longer exposure to altitude the lactate concentration in the muscles and venous blood at a given intensity of exercise(including maximal exertion) is lower, despite the fact that muscle VO2 does not change with adaptation to altitude. To date, there is no universally accepted explanation for this so-called lactate paradox.

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