Guyton and Hall Textbook of Medical Physiology, 12th Ed

CHAPTER 43

Aviation, High Altitude, and Space Physiology

imageAs humans have ascended to higher and higher altitudes in aviation, mountain climbing, and space vehicles, it has become progressively more important to understand the effects of altitude and low gas pressures on the human body. This chapter deals with these problems, as well as acceleratory forces, weightlessness, and other challenges to body homeostasis that occur at high altitude and in space flight.

Effects of Low Oxygen Pressure on the Body

Barometric Pressures at Different Altitudes

Table 43-1 gives the approximate barometric and oxygen pressures at different altitudes, showing that at sea level, the barometric pressure is 760 mm Hg; at 10,000 feet, only 523 mm Hg; and at 50,000 feet, 87 mm Hg. This decrease in barometric pressure is the basic cause of all the hypoxia problems in high-altitude physiology because, as the barometric pressure decreases, the atmospheric oxygen partial pressure (PO2) decreases proportionately, remaining at all times slightly less than 21 percent of the total barometric pressure; at sea level PO2 is about 159 mm Hg, but at 50,000 feet PO2 is only 18 mm Hg.

Table 43-1 Effects of Acute Exposure to Low Atmospheric Pressures on Alveolar Gas Concentrations and Arterial Oxygen Saturation*

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Alveolar Po2 at Different Elevations

Carbon Dioxide and Water Vapor Decrease the Alveolar Oxygen

Even at high altitudes, carbon dioxide is continually excreted from the pulmonary blood into the alveoli. Also, water vaporizes into the inspired air from the respiratory surfaces. These two gases dilute the oxygen in the alveoli, thus reducing the oxygen concentration. Water vapor pressure in the alveoli remains at 47 mm Hg as long as the body temperature is normal, regardless of altitude.

In the case of carbon dioxide, during exposure to very high altitudes, the alveolar PCO2 falls from the sea-level value of 40 mm Hg to lower values. In the acclimatized person, who increases his or her ventilation about fivefold, the PCO2 falls to about 7 mm Hg because of increased respiration.

Now let us see how the pressures of these two gases affect the alveolar oxygen. For instance, assume that the barometric pressure falls from the normal sea-level value of 760 mm Hg to 253 mm Hg, which is the usual measured value at the top of 29,028-foot Mount Everest. Forty-seven mm Hg of this must be water vapor, leaving only 206 mm Hg for all the other gases. In the acclimatized person, 7 mm of the 206 mm Hg must be carbon dioxide, leaving only 199 mm Hg. If there were no use of oxygen by the body, one fifth of this 199 mm Hg would be oxygen and four fifths would be nitrogen; that is, the PO2 in the alveoli would be 40 mm Hg. However, some of this remaining alveolar oxygen is continually being absorbed into the blood, leaving about 35 mm Hg oxygen pressure in the alveoli. At the summit of Mount Everest, only the best of acclimatized people can barely survive when breathing air. But the effect is very different when the person is breathing pure oxygen, as we see in the following discussions.

Alveolar Po2 at Different Altitudes

The fifth column of Table 43-1 shows the approximate PO2s in the alveoli at different altitudes when one is breathing air for both the unacclimatized and the acclimatized person. At sea level, the alveolar PO2is 104 mm Hg; at 20,000 feet altitude, it falls to about 40 mm Hg in the unacclimatized person but only to 53 mm Hg in the acclimatized person. The difference between these two is that alveolar ventilation increases much more in the acclimatized person than in the unacclimatized person, as we discuss later.

Saturation of Hemoglobin with Oxygen at Different Altitudes

Figure 43-1 shows arterial blood oxygen saturation at different altitudes while a person is breathing air and while breathing oxygen. Up to an altitude of about 10,000 feet, even when air is breathed, the arterial oxygen saturation remains at least as high as 90 percent. Above 10,000 feet, the arterial oxygen saturation falls rapidly, as shown by the blue curve of the figure, until it is slightly less than 70 percent at 20,000 feet and much less at still higher altitudes.

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Figure 43-1 Effect of high altitude on arterial oxygen saturation when breathing air and when breathing pure oxygen.

Effect of Breathing Pure Oxygen on Alveolar Po2 at Different Altitudes

When a person breathes pure oxygen instead of air, most of the space in the alveoli formerly occupied by nitrogen becomes occupied by oxygen. At 30,000 feet, an aviator could have an alveolar PO2 as high as 139 mm Hg instead of the 18 mm Hg when breathing air (see Table 43-1).

The red curve of Figure 43-1 shows arterial blood hemoglobin oxygen saturation at different altitudes when one is breathing pure oxygen. Note that the saturation remains above 90 percent until the aviator ascends to about 39,000 feet; then it falls rapidly to about 50 percent at about 47,000 feet.

The “Ceiling” When Breathing Air and When Breathing Oxygen in an Unpressurized Airplane

Comparing the two arterial blood oxygen saturation curves in Figure 43-1, one notes that an aviator breathing pure oxygen in an unpressurized airplane can ascend to far higher altitudes than one breathing air. For instance, the arterial saturation at 47,000 feet when one is breathing oxygen is about 50 percent and is equivalent to the arterial oxygen saturation at 23,000 feet when one is breathing air. In addition, because an unacclimatized person usually can remain conscious until the arterial oxygen saturation falls to 50 percent, for short exposure times the ceiling for an aviator in an unpressurized airplane when breathing air is about 23,000 feet and when breathing pure oxygen is about 47,000 feet, provided the oxygen-supplying equipment operates perfectly.

Acute Effects of Hypoxia

Some of the important acute effects of hypoxia in the unacclimatized person breathing air, beginning at an altitude of about 12,000 feet, are drowsiness, lassitude, mental and muscle fatigue, sometimes headache, occasionally nausea, and sometimes euphoria. These effects progress to a stage of twitchings or seizures above 18,000 feet and end, above 23,000 feet in the unacclimatized person, in coma, followed shortly thereafter by death.

One of the most important effects of hypoxia is decreased mental proficiency, which decreases judgment, memory, and performance of discrete motor movements. For instance, if an unacclimatized aviator stays at 15,000 feet for 1 hour, mental proficiency ordinarily falls to about 50 percent of normal, and after 18 hours at this level it falls to about 20 percent of normal.

Acclimatization to Low Po2

A person remaining at high altitudes for days, weeks, or years becomes more and more acclimatized to the low PO2, so it causes fewer deleterious effects on the body. And it becomes possible for the person to work harder without hypoxic effects or to ascend to still higher altitudes.

The principal means by which acclimatization comes about are (1) a great increase in pulmonary ventilation, (2) increased numbers of red blood cells, (3) increased diffusing capacity of the lungs, (4) increased vascularity of the peripheral tissues, and (5) increased ability of the tissue cells to use oxygen despite low PO2.

Increased Pulmonary Ventilation—Role of Arterial Chemoreceptors

Immediate exposure to low PO2 stimulates the arterial chemoreceptors, and this increases alveolar ventilation to a maximum of about 1.65 times normal. Therefore, compensation occurs within seconds for the high altitude, and it alone allows the person to rise several thousand feet higher than would be possible without the increased ventilation. Then, if the person remains at very high altitude for several days, the chemoreceptors increase ventilation still more, up to about five times normal.

The immediate increase in pulmonary ventilation on rising to a high altitude blows off large quantities of carbon dioxide, reducing the PCO2 and increasing the pH of the body fluids. These changes inhibit the brain stem respiratory center and thereby oppose the effect of low PO2 to stimulate respiration by way of the peripheral arterial chemoreceptors in the carotid and aortic bodies. But during the ensuing 2 to 5 days, this inhibition fades away, allowing the respiratory center to respond with full force to the peripheral chemoreceptor stimulus from hypoxia, and ventilation increases to about five times normal.

The cause of this fading inhibition is believed to be mainly a reduction of bicarbonate ion concentration in the cerebrospinal fluid, as well as in the brain tissues. This in turn decreases the pH in the fluids surrounding the chemosensitive neurons of the respiratory center, thus increasing the respiratory stimulatory activity of the center.

An important mechanism for the gradual decrease in bicarbonate concentration is compensation by the kidneys for the respiratory alkalosis, as discussed in Chapter 30. The kidneys respond to decreased PCO2by reducing hydrogen ion secretion and increasing bicarbonate excretion. This metabolic compensation for the respiratory alkalosis gradually reduces plasma and cerebrospinal fluid bicarbonate concentration and pH toward normal and removes part of the inhibitory effect on respiration of low hydrogen ion concentration. Thus, the respiratory centers are much more responsive to the peripheral chemoreceptor stimulus caused by the hypoxia after the kidneys compensate for the alkalosis.

Increase in Red Blood Cells and Hemoglobin Concentration During Acclimatization

As discussed in Chapter 32, hypoxia is the principal stimulus for causing an increase in red blood cell production. Ordinarily, when a person remains exposed to low oxygen for weeks at a time, the hematocrit rises slowly from a normal value of 40 to 45 to an average of about 60, with an average increase in whole blood hemoglobin concentration from normal of 15 g/dl to about 20 g/dl.

In addition, the blood volume also increases, often by 20 to 30 percent, and this increase times the increased blood hemoglobin concentration gives an increase in total body hemoglobin of 50 or more percent.

Increased Diffusing Capacity After Acclimatization

The normal diffusing capacity for oxygen through the pulmonary membrane is about 21 ml/mm Hg/min, and this diffusing capacity can increase as much as threefold during exercise. A similar increase in diffusing capacity occurs at high altitude.

Part of the increase results from increased pulmonary capillary blood volume, which expands the capillaries and increases the surface area through which oxygen can diffuse into the blood. Another part results from an increase in lung air volume, which expands the surface area of the alveolar-capillary interface still more. A final part results from an increase in pulmonary arterial blood pressure; this forces blood into greater numbers of alveolar capillaries than normally—especially in the upper parts of the lungs, which are poorly perfused under usual conditions.

Peripheral Circulatory System Changes During Acclimatization—Increased Tissue Capillarity

The cardiac output often increases as much as 30 percent immediately after a person ascends to high altitude but then decreases back toward normal over a period of weeks as the blood hematocrit increases, so the amount of oxygen transported to the peripheral body tissues remains about normal.

Another circulatory adaptation is growth of increased numbers of systemic circulatory capillaries in the nonpulmonary tissues, which is called increased tissue capillarity (or angiogenesis). This occurs especially in animals born and bred at high altitudes but less so in animals that later in life become exposed to high altitude.

In active tissues exposed to chronic hypoxia, the increase in capillarity is especially marked. For instance, capillary density in right ventricular muscle increases markedly because of the combined effects of hypoxia and excess workload on the right ventricle caused by pulmonary hypertension at high altitude.

Cellular Acclimatization

In animals native to altitudes of 13,000 to 17,000 feet, cell mitochondria and cellular oxidative enzyme systems are slightly more plentiful than in sea-level inhabitants. Therefore, it is presumed that the tissue cells of high altitude–acclimatized human beings also can use oxygen more effectively than can their sea-level counterparts.

Natural Acclimatization of Native Human Beings Living at High Altitudes

Many native human beings in the Andes and in the Himalayas live at altitudes above 13,000 feet—one group in the Peruvian Andes lives at an altitude of 17,500 feet and works a mine at an altitude of 19,000 feet. Many of these natives are born at these altitudes and live there all their lives. In all aspects of acclimatization, the natives are superior to even the best-acclimatized lowlanders, even though the lowlanders might also have lived at high altitudes for 10 or more years. Acclimatization of the natives begins in infancy. The chest size, especially, is greatly increased, whereas the body size is somewhat decreased, giving a high ratio of ventilatory capacity to body mass. In addition, their hearts, which from birth onward pump extra amounts of cardiac output, are considerably larger than the hearts of lowlanders.

Delivery of oxygen by the blood to the tissues is also highly facilitated in these natives. For instance, Figure 43-2 shows oxygen-hemoglobin dissociation curves for natives who live at sea level and for their counterparts who live at 15,000 feet. Note that the arterial oxygen PO2 in the natives at high altitude is only 40 mm Hg, but because of the greater quantity of hemoglobin, the quantity of oxygen in their arterial blood is greater than that in the blood of the natives at the lower altitude. Note also that the venous PO2 in the high-altitude natives is only 15 mm Hg less than the venous PO2 for the lowlanders, despite the very low arterial PO2, indicating that oxygen transport to the tissues is exceedingly effective in the naturally acclimatized high-altitude natives.

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Figure 43-2 Oxygen-hemoglobin dissociation curves for blood of high-altitude residents (red curve) and sea-level residents (blue curve), showing the respective arterial and venous PO2 levels and oxygen contents as recorded in their native surroundings.

(Data from Oxygen-dissociation curves for bloods of high-altitude and sea-level residents. PAHO Scientific Publication No. 140, Life at High Altitudes, 1966.)

Reduced Work Capacity at High Altitudes and Positive Effect of Acclimatization

In addition to the mental depression caused by hypoxia, as discussed earlier, the work capacity of all muscles is greatly decreased in hypoxia. This includes not only skeletal muscles but also cardiac muscles.

In general, work capacity is reduced in direct proportion to the decrease in maximum rate of oxygen uptake that the body can achieve.

To give an idea of the importance of acclimatization in increasing work capacity, consider the large differences in work capacities as percent of normal for unacclimatized and acclimatized people at an altitude of 17,000 feet:

 

Work capacity (percent of normal)

Unacclimatized

50

Acclimatized for 2 months

68

Native living at 13,200 feet but working at 17,000 feet

87

Thus, naturally acclimatized native persons can achieve a daily work output even at high altitude almost equal to that of a lowlander at sea level, but even well-acclimatized lowlanders can almost never achieve this result.

Acute Mountain Sickness and High-Altitude Pulmonary Edema

A small percentage of people who ascend rapidly to high altitudes become acutely sick and can die if not given oxygen or removed to a low altitude. The sickness begins from a few hours up to about 2 days after ascent. Two events frequently occur:

1. Acute cerebral edema. This is believed to result from local vasodilation of the cerebral blood vessels, caused by the hypoxia. Dilation of the arterioles increases blood flow into the capillaries, thus increasing capillary pressure, which in turn causes fluid to leak into the cerebral tissues. The cerebral edema can then lead to severe disorientation and other effects related to cerebral dysfunction.

2. Acute pulmonary edema. The cause of this is still unknown, but one explanation is the following: The severe hypoxia causes the pulmonary arterioles to constrict potently, but the constriction is much greater in some parts of the lungs than in other parts, so more and more of the pulmonary blood flow is forced through fewer and fewer still unconstricted pulmonary vessels. The postulated result is that the capillary pressure in these areas of the lungs becomes especially high and local edema occurs. Extension of the process to progressively more areas of the lungs leads to spreading pulmonary edema and severe pulmonary dysfunction that can be lethal. Allowing the person to breathe oxygen usually reverses the process within hours.

Chronic Mountain Sickness

Occasionally, a person who remains at high altitude too long develops chronic mountain sickness, in which the following effects occur: (1) The red cell mass and hematocrit become exceptionally high, (2) the pulmonary arterial pressure becomes elevated even more than the normal elevation that occurs during acclimatization, (3) the right side of the heart becomes greatly enlarged, (4) the peripheral arterial pressure begins to fall, (5) congestive heart failure ensues, and (6) death often follows unless the person is removed to a lower altitude.

The causes of this sequence of events are probably threefold: First, the red cell mass becomes so great that the blood viscosity increases severalfold; this increased viscosity tends to decrease tissue blood flow so that oxygen delivery also begins to decrease. Second, the pulmonary arterioles become vasoconstricted because of the lung hypoxia. This results from the hypoxic vascular constrictor effect that normally operates to divert blood flow from low-oxygen to high-oxygen alveoli, as explained in Chapter 38. But because all the alveoli are now in the low-oxygen state, all the arterioles become constricted, the pulmonary arterial pressure rises excessively, and the right side of the heart fails. Third, the alveolar arteriolar spasm diverts much of the blood flow through nonalveolar pulmonary vessels, thus causing an excess of pulmonary shunt blood flow where the blood is poorly oxygenated; this further compounds the problem. Most of these people recover within days or weeks when they are moved to a lower altitude.

Effects of Acceleratory Forces on the Body in Aviation and Space Physiology

Because of rapid changes in velocity and direction of motion in airplanes or spacecraft, several types of acceleratory forces affect the body during flight. At the beginning of flight, simple linear acceleration occurs; at the end of flight, deceleration; and every time the vehicle turns, centrifugal acceleration.

Centrifugal Acceleratory Forces

When an airplane makes a turn, the force of centrifugal acceleration is determined by the following relation:

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in which f is centrifugal acceleratory force, m is the mass of the object, v is velocity of travel, and r is radius of curvature of the turn. From this formula, it is obvious that as the velocity increases, the force of centrifugal acceleration increases in proportion to the square of the velocity. It is also obvious that the force of acceleration is directly proportional to the sharpness of the turn (the less the radius).

Measurement of Acceleratory Force—“G.”

When an aviator is simply sitting in his seat, the force with which he is pressing against the seat results from the pull of gravity and is equal to his weight. The intensity of this force is said to be +1G because it is equal to the pull of gravity. If the force with which he presses against the seat becomes five times his normal weight during pull-out from a dive, the force acting on the seat is +5 G.

If the airplane goes through an outside loop so that the person is held down by his seat belt, negative G is applied to his body; if the force with which he is held down by his belt is equal to the weight of his body, the negative force is −1G.

Effects of Centrifugal Acceleratory Force on the Body—(Positive G)

Effects on the Circulatory System

The most important effect of centrifugal acceleration is on the circulatory system, because blood is mobile and can be translocated by centrifugal forces.

When an aviator is subjected to positive G, blood is centrifuged toward the lowermost part of the body. Thus, if the centrifugal acceleratory force is +5 G and the person is in an immobilized standing position, the pressure in the veins of the feet becomes greatly increased (to about 450 mm Hg). In the sitting position, the pressure becomes nearly 300 mm Hg. And, as pressure in the vessels of the lower body increases, these vessels passively dilate so that a major portion of the blood from the upper body is translocated into the lower vessels. Because the heart cannot pump unless blood returns to it, the greater the quantity of blood “pooled” in this way in the lower body, the less that is available for the cardiac output.

Figure 43-3 shows the changes in systolic and diastolic arterial pressures (top and bottom curves, respectively) in the upper body when a centrifugal acceleratory force of +3.3 G is suddenly applied to a sitting person. Note that both these pressures fall below 22 mm Hg for the first few seconds after the acceleration begins but then return to a systolic pressure of about 55 mm Hg and a diastolic pressure of 20 mm Hg within another 10 to 15 seconds. This secondary recovery is caused mainly by activation of the baroreceptor reflexes.

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Figure 43-3 Changes in systolic (top of curve) and diastolic (bottom of curve) arterial pressures after abrupt and continuing exposure of a sitting person to an acceleratory force from top to bottom of 3.3 G.

(Data from Martin EE, Henry JP: Effects of time and temperature upon tolerance to positive acceleration. J Aviation Med 22:382, 1951.)

Acceleration greater than 4 to 6 G causes “blackout” of vision within a few seconds and unconsciousness shortly thereafter. If this great degree of acceleration is continued, the person will die.

Effects on the Vertebrae

Extremely high acceleratory forces for even a fraction of a second can fracture the vertebrae. The degree of positive acceleration that the average person can withstand in the sitting position before vertebral fracture occurs is about 20 G.

Negative G

The effects of negative G on the body are less dramatic acutely but possibly more damaging permanently than the effects of positive G. An aviator can usually go through outside loops up to negative acceleratory forces of −4 to −5 G without causing permanent harm, although causing intense momentary hyperemia of the head. Occasionally, psychotic disturbances lasting for 15 to 20 minutes occur as a result of brain edema.

Occasionally, negative G forces can be so great (−20 G, for instance) and centrifugation of the blood into the head is so great that the cerebral blood pressure reaches 300 to 400 mm Hg, sometimes causing small vessels on the surface of the head and in the brain to rupture. However, the vessels inside the cranium show less tendency for rupture than would be expected for the following reason: The cerebrospinal fluid is centrifuged toward the head at the same time that blood is centrifuged toward the cranial vessels, and the greatly increased pressure of the cerebrospinal fluid acts as a cushioning buffer on the outside of the brain to prevent intracerebral vascular rupture.

Because the eyes are not protected by the cranium, intense hyperemia occurs in them during strong negative G. As a result, the eyes often become temporarily blinded with “red-out.”

Protection of the Body Against Centrifugal Acceleratory Forces

Specific procedures and apparatus have been developed to protect aviators against the circulatory collapse that might occur during positive G. First, if the aviator tightens his or her abdominal muscles to an extreme degree and leans forward to compress the abdomen, some of the pooling of blood in the large vessels of the abdomen can be prevented, delaying the onset of blackout. Also, special “anti-G” suits have been devised to prevent pooling of blood in the lower abdomen and legs. The simplest of these applies positive pressure to the legs and abdomen by inflating compression bags as the G increases. Theoretically, a pilot submerged in a tank or suit of water might experience little effect of G forces on the circulation because the pressures developed in the water pressing on the outside of the body during centrifugal acceleration would almost exactly balance the forces acting in the body. However, the presence of air in the lungs still allows displacement of the heart, lung tissues, and diaphragm into seriously abnormal positions despite submersion in water. Therefore, even if this procedure were used, the limit of safety almost certainly would still be less than 10 G.

Effects of Linear Acceleratory Forces on the Body

Acceleratory Forces in Space Travel

Unlike an airplane, a spacecraft cannot make rapid turns; therefore, centrifugal acceleration is of little importance except when the spacecraft goes into abnormal gyrations. However, blast-off acceleration and landing deceleration can be tremendous; both of these are types of linear acceleration, one positive and the other negative.

Figure 43-4 shows an approximate profile of acceleration during blast-off in a three-stage spacecraft, demonstrating that the first-stage booster causes acceleration as high as 9 G, and the second-stage booster as high as 8 G. In the standing position, the human body could not withstand this much acceleration, but in a semireclining position transverse to the axis of acceleration, this amount of acceleration can be withstood with ease despite the fact that the acceleratory forces continue for as long as several minutes at a time. Therefore, we see the reason for the reclining seats used by astronauts.

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Figure 43-4 Acceleratory forces during takeoff of a spacecraft.

Problems also occur during deceleration when the spacecraft re-enters the atmosphere. A person traveling at Mach 1 (the speed of sound and of fast airplanes) can be safely decelerated in a distance of about 0.12 mile, whereas a person traveling at a speed of Mach 100 (a speed possible in interplanetary space travel) would require a distance of about 10,000 miles for safe deceleration. The principal reason for this difference is that the total amount of energy that must be dispelled during deceleration is proportional to the square of the velocity, which alone increases the required distance for decelerations between Mach 1 versus Mach 100 about 10,000-fold. Therefore, deceleration must be accomplished much more slowly from high velocities than is necessary at lower velocities.

Deceleratory Forces Associated with Parachute Jumps

When the parachuting aviator leaves the airplane, his velocity of fall is at first exactly 0 feet per second. However, because of the acceleratory force of gravity, within 1 second his velocity of fall is 32 feet per second (if there is no air resistance); in 2 seconds it is 64 feet per second; and so on. As the velocity of fall increases, the air resistance tending to slow the fall also increases. Finally, the deceleratory force of the air resistance exactly balances the acceleratory force of gravity, so after falling for about 12 seconds, the person will be falling at a “terminal velocity” of 109 to 119 miles per hour (175 feet per second). If the parachutist has already reached terminal velocity before opening his parachute, an “opening shock load” of up to 1200 pounds can occur on the parachute shrouds.

The usual-sized parachute slows the fall of the parachutist to about one-ninth the terminal velocity. In other words, the speed of landing is about 20 feet per second, and the force of impact against the earth is 1/81 the impact force without a parachute. Even so, the force of impact is still great enough to cause considerable damage to the body unless the parachutist is properly trained in landing. Actually, the force of impact with the earth is about the same as that which would be experienced by jumping without a parachute from a height of about 6 feet. Unless forewarned, the parachutist will be tricked by his senses into striking the earth with extended legs, and this will result in tremendous deceleratory forces along the skeletal axis of the body, resulting in fracture of his pelvis, vertebrae, or leg. Consequently, the trained parachutist strikes the earth with knees bent but muscles taut to cushion the shock of landing.

“Artificial Climate” in the Sealed Spacecraft

Because there is no atmosphere in outer space, an artificial atmosphere and climate must be produced in a spacecraft. Most important, the oxygen concentration must remain high enough and the carbon dioxide concentration low enough to prevent suffocation. In some earlier space missions, a capsule atmosphere containing pure oxygen at about 260 mm Hg pressure was used, but in the modern space shuttle, gases about equal to those in normal air are used, with four times as much nitrogen as oxygen and a total pressure of 760 mm Hg. The presence of nitrogen in the mixture greatly diminishes the likelihood of fire and explosion. It also protects against development of local patches of lung atelectasis that often occur when breathing pure oxygen because oxygen is absorbed rapidly when small bronchi are temporarily blocked by mucous plugs.

For space travel lasting more than several months, it is impractical to carry along an adequate oxygen supply. For this reason, recycling techniques have been proposed for use of the same oxygen over and over again. Some recycling processes depend on purely physical procedures, such as electrolysis of water to release oxygen. Others depend on biological methods, such as use of algae with their large store of chlorophyll to release oxygen from carbon dioxide by the process of photosynthesis. A completely satisfactory system for recycling has yet to be achieved.

Weightlessness in Space

A person in an orbiting satellite or a nonpropelled spacecraft experiences weightlessness, or a state of near-zero G force, which is sometimes called microgravity. That is, the person is not drawn toward the bottom, sides, or top of the spacecraft but simply floats inside its chambers. The cause of this is not failure of gravity to pull on the body because gravity from any nearby heavenly body is still active. However, the gravity acts on both the spacecraft and the person at the same time so that both are pulled with exactly the same acceleratory forces and in the same direction. For this reason, the person simply is not attracted toward any specific wall of the spacecraft.

Physiologic Problems of Weightlessness (Microgravity)

The physiologic problems of weightlessness have not proved to be of much significance, as long as the period of weightlessness is not too long. Most of the problems that do occur are related to three effects of the weightlessness: (1) motion sickness during the first few days of travel, (2) translocation of fluids within the body because of failure of gravity to cause normal hydrostatic pressures, and (3) diminished physical activity because no strength of muscle contraction is required to oppose the force of gravity.

Almost 50 percent of astronauts experience motion sickness, with nausea and sometimes vomiting, during the first 2 to 5 days of space travel. This probably results from an unfamiliar pattern of motion signals arriving in the equilibrium centers of the brain, and at the same time lack of gravitational signals.

The observed effects of prolonged stay in space are the following: (1) decrease in blood volume, (2) decrease in red blood cell mass, (3) decrease in muscle strength and work capacity, (4) decrease in maximum cardiac output, and (5) loss of calcium and phosphate from the bones, as well as loss of bone mass. Most of these same effects also occur in people who lie in bed for an extended period of time. For this reason, exercise programs are carried out by astronauts during prolonged space missions.

In previous space laboratory expeditions in which the exercise program had been less vigorous, the astronauts had severely decreased work capacities for the first few days after returning to earth. They also tended to faint (and still do, to some extent) when they stood up during the first day or so after return to gravity because of diminished blood volume and diminished responses of the arterial pressure control mechanisms.

Cardiovascular, Muscle, and Bone “Deconditioning” During Prolonged Exposure to Weightlessness

During very long space flights and prolonged exposure to microgravity, gradual “deconditioning” effects occur on the cardiovascular system, skeletal muscles, and bone despite rigorous exercise during the flight. Studies of astronauts on space flights lasting several months have shown that they may lose as much 1.0 percent of their bone mass each month even though they continue to exercise. Substantial atrophy of cardiac and skeletal muscles also occurs during prolonged exposure to a microgravity environment.

One of the most serious effects is cardiovascular “deconditioning,” which includes decreased work capacity, reduced blood volume, impaired baroreceptor reflexes, and reduced orthostatic tolerance. These changes greatly limit the astronauts’ ability to stand upright or perform normal daily activities after returning to the full gravity of Earth.

Astronauts returning from space flights lasting 4 to 6 months are also susceptible to bone fractures and may require several weeks before they return to preflight cardiovascular, bone, and muscle fitness. As space flights become longer in preparation for possible human exploration of other planets, such as Mars, the effects of prolonged microgravity could pose a very serious threat to astronauts after they land, especially in the event of an emergency landing. Therefore, considerable research effort has been directed toward developing countermeasures, in addition to exercise, that can prevent or more effectively attenuate these changes. One such countermeasure that is being tested is the application of intermittent “artificial gravity” caused by short periods (e.g., 1 hour each day) of centrifugal acceleration of the astronauts while they sit in specially designed short-arm centrifuges that create forces of up to 2 to 3 G.

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