SPACE, RESPIRATORY SYSTEM 113
Humbert M, Morrell NW, Archer SL, et al. (2004) Cellular and
molecular pathobiology of pulmonary arterial hypertension.
Journal of the American College of Cardiology 43: 13S–24S.
Jeffery TK and Wanstall JC (2001) Pulmonary vascular remodeling: a target for therapeutic intervention in pulmonary hypertension. Pharmacology and Therapeutics 92: 1–20.
Liu C, Nath KA, Katusic ZS, and Caplice NM (2004) Smooth
muscle progenitor cells in vascular disease. Trends in Cardiovascular Medicine 14: 288–293.
Mandegar M, Fung YB, and Huang W (2004) Cellular and molecular mechanisms of pulmonary vascular remodeling: role in
the development of pulmonary hypertension. Microvascular Research 68: 75–103.
Owens GK (1995) Regulation of differentiation of vascular
smooth muscle cells. Physiology Reviews 75: 487–517.
Pass SE and Dusing ML (2002) Current and emerging therapy for
primary pulmonary hypertension. Annals of Pharmacotherapy
36: 1414–1422.
Shanahan CM and Weissberg PL (1998) Smooth muscle cell heterogeneity: patterns of gene expression in vascular smooth muscle cells in vitro and in vivo. Atherosclerosis, Thrombosis and
Vascular Biology 18: 333–338.
Strange JW, Wharton J, Phillips PG, and Wilkins MR (2002)
Recent insights into the pathogenesis and therapeutics of
pulmonary hypertension. Clinical Science 102: 253–268.
SPACE, RESPIRATORY SYSTEM
G K Prisk, University of California – San Diego, La
Jolla, CA, USA
& 2006 Elsevier Ltd. All rights reserved.
Abstract
The lung is extremely sensitive to gravity, which induces large
regional differences in ventilation, blood flow, and gas exchange
in normal subjects. Functional residual capacity is reduced in the
absence of gravity, as is residual volume, although by different
mechanisms. While the removal of gravity greatly reduces the
unevenness of both ventilation and perfusion in the lung, there
are only minor changes in the degree of ventilation–perfusion
inequality in microgravity (mG), suggesting a mechanism by
which gravity serves to match ventilation to perfusion, making
for a more efficient lung in 1G than might otherwise be anticipated. Despite some early predictions to the contrary, the lung
does not become edematous in mG, and there is no apparent
disruption to gas exchange. mG reduces the hypoxic, but
not the hypercapnic, ventilatory response. Studies convincingly
show that sleep disturbances in mG are not a result of respiratoryrelated events, and that obstructive sleep apnea is principally
caused by the gravitational effects on the upper airways. Aerosol
deposition in the lung is reduced in mG. However, aerosols may
be deposited more peripherally, which may place the lung at risk
in the reduced gravity environments of the Moon and Mars,
which are likely to have reactive dust species on their surfaces.
Gravity, the Lung, and Space Flight
Although there is little, if any, structural difference
between the top and bottom of the normal human
lung, there are marked functional differences caused
by the effects of gravity (Table 1). For example, the
alveoli at the top of the lung are relatively overexpanded compared to the bottom of the lung because the weight of the dependent portions of the
lung stretches the upper portions. As a consequence
of this, ventilation is higher at the bottom of the lung,
because the initial smaller volume there makes the
lung more readily able to expand in response to a
given breathing effort.
The pulmonary vascular system operates at a
relatively low pressure compared to the systemic circulation and, as a consequence, hydrostatic effects
strongly influence the vertical distribution of blood
flow in the normal human lung, with much greater
flows near the bases than the apices. Because the
differences in perfusion are larger than those in ventilation, the ventilation–perfusion ratio is higher at
the top than the bottom of the lung. Since it is
the ventilation–perfusion ratio that determines gas
exchange, regional differences in alveolar gas and
effluent blood composition occur.
Making Measurements in Microgravity
There are only two practical methods of achieving
microgravity suitable for human experimentation:
parabolic flight in aircraft and space flight. Parabolic
flight provides only short periods of microgravity
(typically B25 s), and these are usually sandwiched
between periods of hypergravity. Any measurements
made in parabolic flight are therefore subject to the
effects that may ensue from this period of hypergravity. In contrast, spaceflight provides sustained
microgravity (typically from about 1 week to more
than 1 year at present) but flight opportunities are
infrequent at best.
Skylab provided the first real opportunity to conduct pulmonary function measurements in space,
but ground simulation studies showed that some of
the changes observed may have at least been partly
due to the atmospheric conditions (5 psia, B345 kPa
or B260 mmHg, 70% O2) in the vehicle rather
than microgravity per se. In contrast, more recent
spacecraft (the Space Shuttle, the now-defunct
114 SPACE, RESPIRATORY SYSTEM
Table 1 The effect of microgravity on various aspects of lung function
Aspect of lung function
Change with microgravity
Lung volumes and pulmonary mechanics
Vital capacity
Slight initial reduction early inflight, probably due to increased intrathoracic blood volume, but
unchanged from 1G thereafter
Functional residual capacity
Reduced by B15%; intermediate between standing and supine in 1G
Residual volume
Reduced by B18%; probably due to elimination of apicobasal gradients in lung expansion
Tidal volume
Reduced by B15%
Respiratory frequency
Increased by B9%
Forced expiratory flows
Initial decrease in peak expiratory flow at the onset of mG, with a subsequent return to normal
after 4–5 days; no change in flows at low lung volumes
Chest and abdominal mechanics
Increased abdominal compliance (B30%); decrease in EMG activity of the ribcage
Pulmonary ventilation
Airway closure
Large-scale inhomogeneity
Small-scale inhomogeneity
Pulmonary perfusion and fluid
balance
Cardiac output
Diffusing capacity
Lung water
Distribution of pulmonary perfusion
Still occurs at approximately the same absolute lung volume
Greatly reduced in vital capacity breaths; largely unchanged in tidal volume breaths
Persists, although with some changes in acinar conformation, probably due to changes in lung
fluid balance
Initial increase of B35% at the onset of mG with subsequent decrease, but remaining above 1G
levels; some suggestion of subsequent increase after more than 2 weeks in mG
Increases by B28% and remains unaltered for duration of mG exposure due to increases in both
pulmonary capillary blood volume and surface area available for gas exchange
Unchanged at the onset of mG, but decreased after some days
More uniform, probably due to abolition of top-to-bottom gradients in blood flow, but with
persisting inhomogeneity
Pulmonary gas exchange
Resting gas exchange
Total ventilation
Alveolar ventilation
End-tidal gas concentrations
Unchanged O2 consumption and CO2 production
Slightly decreased (B7%)
Unchanged
PO2 unchanged, PCO2 may be slightly increased probably due to increased environmental CO2
Inequality of ventilation-perfusion
ratio
Evidence for reduction in top-to-bottom gradients, but persisting inequality in face of reductions in
inequality of both ventilation and perfusion
Response to exercise
Ventilatory response
Cardiac response
Largely unchanged
Reduced increase in cardiac output for a given O2 consumption requirement
Ventilatory control
Isocapnic hypoxic ventilatory
response
Hypercapnic ventilatory response
Largely unchanged
Sleep-disordered breathing
Apnea-hypopnea index
Snoring
Respiratory-related arousals
Significantly reduced
Reduced
Virtually eliminated
Aerosol deposition
Magnitude
Location
Reduced due to absence of sedimentation, but unexpectedly high for small particles
Probably more peripheral
Extra-vehicular activity
Ventilation-perfusion ratios
Unaltered 24 h after EVA compared to before (all measurements in mG)
Approximately halved; equivalent to that supine in 1G
Except where noted the comparison is made with the upright position in 1G.
Russian space station Mir, and the International
Space Station (ISS)) have provided researchers with a
normoxic, normobaric environment. Since 1983, the
US Space Shuttle has, at times, carried the European
built Spacelab in the cargo bay, and subsequently the
commercially built Spacehab. Shuttle flights are limited to missions of short duration (the maximum
currently being about 17 days), and so necessarily
deal with only acute phases of the adaptation to
microgravity. Longer duration missions now occur on
SPACE, RESPIRATORY SYSTEM 115
the ISS and prior to that on Mir, Salyut, and Skylab.
However, populations available for study are small,
and in experiments involving human subjects, the
design must often be such that statistically viable results can be achieved using only an n of 4. Typically,
in such experiments subjects act as their own control,
with extensive preflight and postflight testing.
Normal Physiology in Microgravity
Lung Volumes and Chest Wall Mechanics
A study of lung volumes in microgravity (mG) performed in Skylab showed a B10% decrease in vital
capacity. However, ground controls using a comparable atmosphere showed a 3–5% reduction, suggesting a confounding effect of the hypobaric
environment. During the 1991 flight of Spacelab Life
Sciences-1 (SLS-1), vital capacity showed a B5%
reduction early in flight (Flight Day 2, FD-2) compared to that standing in 1G. However, by FD-4 the
reduction had been abolished. An early inflight increase in intrathoracic blood volume, with a subsequent reduction as plasma volume is reduced, seems
the most plausible explanation for these results.
Functional residual capacity (FRC) decreased by
B15% in mG compared to that of the standing subject
in 1G. This reduction was largely in line with predictions of a B10% decrease, primarily based on
a cranial shift of the diaphragm and abdominal contents as gravity was removed (a potentially large effect
that would decrease FRC), an outward movement
of the ribcage, and an upward movement of the
shoulder girdle (both small effects that would increase
FRC). As expected, the FRC in mG was intermediate
to that measured standing and supine in 1G.
Residual volume (RV) is generally quite resistant to
change. Transitions between upright and supine, and
water immersion typically result in no significant decrease in RV. However, in sustained mG, RV was
markedly decreased by B18% (310 ml) compared to
standing and was also significantly below that measured supine. In 1G, when lung volume is reduced below FRC, airways closure begins in the more
gravitationally dependent lung regions (because of distortion of the lung by its own weight), and this airways
closure progresses up the lung until RV is reached, resulting in a large difference in regional RV between the
top and bottom of the lung in 1G. However, in mG the
apico-basal gradients in regional lung volume due to
gravity are abolished, resulting in the regional volume
of lung units being much more uniform, reducing RV.
It is reasonable to expect that removal of gravity
may result in some alterations in local airway stress,
and thus in expiratory flow limitation. Studies in
parabolic flight showed effects consistent with an increase in intrathoracic blood volume, altering elastic
recoil (a scooping out of the MEFV curve at low lung
volumes) similar to changes seen in recumbency and
immersion. However, in space flight there were no
discernable changes in the shape of the MEFV curve
at low lung volumes, suggesting little, if any, change in
the behavior of the central and peripheral airways.
The mechanical properties of the lung and chest
wall have only been studied in parabolic flight. There
is a headward displacement of the diaphragm with
an inward displacement of the abdominal wall reducing lung volume, and an increase in abdominal
wall compliance. However there is also a decrease in
the EMG activity of the muscles that activate the
upper portion of the ribcage. This may be part of the
operational length compensation reflex in which as
the length of the diaphragm increases, there is a
compensatory decrease in the activation of the other
inspiratory muscles keeping tidal volume constant.
Pulmonary Ventilation
Vital capacity single breath nitrogen washout (SBW)
tests showed marked reductions in the height of the
terminal rise in N2, and in cardiogenic oscillations
(both markers of large-scale ventilatory inhomogeneity), but a clear persistence nevertheless, suggesting
a considerable contribution from nongravitational
factors. The onset of airways closure occurred at the
same absolute lung volume in 1G and mG, consistent
with the suggestion of ‘patchy’ airways closure occurring at a similar absolute lung volume regardless
of the gravitational distortion of the lung.
Multiple breath washouts (MBWs) using near tidal
volume breaths showed few significant changes between standing data in 1G and mG. This surprising
result led to the conclusion that the primary determinants of large-scale ventilatory inhomogeneity
during tidal breathing in the upright posture were
not primarily gravitational in origin.
While there was good reason to suspect that
large-scale inhomogeneity should be subject to considerable alteration in mG, there was generally no
consideration that small-scale inhomogeneity should
be affected. The SBW performed in space flight confirmed previous observations from parabolic flight
that phase III slope (predominately a marker of
small-scale inhomogeneity) was only slightly reduced
by the removal of gravity (B25%).
Small-scale effects can be studied by performing
SBWs in which trace quantities of helium (He, a
rapidly diffusing gas) and sulfur hexafluoride (SF6, a
slowly diffusing gas) are included in the inspired test
gas. At the level of the acinus, diffusion takes over
116 SPACE, RESPIRATORY SYSTEM
from convection as the principal mechanism of gas
transport, and it is the interaction between these different transport processes that generates the inhomogeneity of ventilation. In normal humans in 1G,
SF6 exhibits a steeper phase III slope than does He
because of the structure of the human acinus, and
because the more rapid diffusion of He serves to
more readily abolish any concentration gradients.
In space flight, the He and SF6 slope became the
same in mG, and the slope for SF6 actually became
flatter than that for He following a breathhold, similar to that seen in heart-lung transplant recipients
undergoing acute rejection episodes. In that case,
conformational changes near the entrance of the acinus, probably as a result of acute inflammation, were
the cause. However, in space flight the effect was
rapidly reversible, as the phase III slope difference
had returned to preflight values within 6–10 h of
landing, and the effect was absent in tests performed
in parabolic flight, suggesting that it takes some time
to develop. Recent observations in steep (601) headdown tilt, which raises pulmonary capillary pressures, suggest a role of changes in the distribution
of lung water on acinar conformation, but these
conclusions are preliminary at best.
Cardiac Output
Cardiac output rises by approximately 35% above
preflight standing levels 24 h after the onset of mG,
and then decreases subsequently. This is accompanied by a slight bradycardia and, as a result, stroke
volume is increased by 60–70% early in flight, and
also shows a subsequent decrease. However, some
data suggest that cardiac output may rise again after
B2 weeks in mG due to an increase in heart rate in
the face of a constant stroke volume, but to date
there have been no studies in mG of longer duration
to support these observations.
These increases in cardiac output occur in the face
of significant decreases in cardiac filling pressures
inferred from central venous pressure (CVP) measurements using catheters in the superior vena cava.
Since the changes in CVP occur within seconds of the
removal of gravity, it seems highly unlikely that there
is any change in cardiac muscle performance per se.
Thus, cardiac transmural pressure must have increased, presumably due to a decrease in extracardiac pressure, which is probably similar to pleural
pressure. The fact that FRC decreases upon entry
into mG (increasing in pleural pressure) suggests that
local pressure changes must be considered when
considering cardiac performance, although a clear
understanding of the seemingly contradictory results
is not yet available.
Diffusing Capacity and Lung Water
The single-breath diffusing capacity for carbon monoxide (DLco) rose substantially (28%) on exposure to
mG and remained elevated over the course of a 9-day
flight. This was a result of parallel increases in both
pulmonary capillary blood volume (Vc, 28%) and
membrane diffusing capacity (Dm, 27%). There was
a rapid return to preflight conditions after return to
1G. The changes in DLco and its components were
attributed to a more uniform filling of the pulmonary
capillary bed with an attendant increase in the surface area available for gas exchange.
The possibility of pulmonary edema formation in
mG caused by a headward shift of fluid, and what was
at the time a presumed increase in central venous
pressure, had previously been suggested. If edema had
occurred, a decrease in either DLco or Dm might have
been expected early in flight with increases later as
the edema resolved, but this was not the case. Pulmonary tissue volume measured using soluble gas
uptake (which is sensitive to extravascular fluid in the
lungs) was unchanged after 24 h of mG and was 20–
25% lower after 9 days, despite increases in thoracic
blood volume, although these measurements are
taken from only a few subjects. These results are
consistent with observations of the low compliance of
the pulmonary interstitium, which in the presence of
a fall in central venous pressure would be expected to
result in a gradual reduction in fluid in these tissues.
Pulmonary Perfusion
There are no direct measurements of the distribution
of pulmonary blood flow during space flight, principally because of the technical challenges of such
measurements. Some imaging studies using injected
radioactive microaggregates in humans or microspheres in animals have been performed in parabolic
flight, and these show a clear influence of gravity,
albeit with a considerable degree of nongravitational
influence as well. A technique similar to a SBW test
using evolved CO2 as the tracer gas has been used in
parabolic flight and space flight to provide estimate
inhomogeneity of perfusion. In this technique, the
presence of cardiogenic oscillations provides evidence for differences in perfusion between areas of
the lung proximal and distal to the heart, while the
fall in CO2 after airways closure is evidence for a
lower CO2 (and thus lower blood flow) in the upper
part of the lung in 1G.
In 1G, there are prominent cardiogenic oscillations, and a marked fall in CO2 towards the end
of exhalation, consistent with the known vertical
gradient of pulmonary blood flow. In parabolic
flight, there was no terminal fall, and it was found
SPACE, RESPIRATORY SYSTEM 117
that the size of the cardiogenic oscillations depended
strongly on gravity with small but measurable values
in mG. In sustained mG, the size of the cardiogenic
oscillations was decreased to a similar degree to
that supine (B60% standing), while the terminal fall
was absent, consistent with parabolic flight. Since
airways closure still occurs in mG, the absence of a
terminal fall of CO2 means that the blood flow in the
regions of lung behind airways that close, and in the
regions of lung behind airways that remain open,
must be similar, consistent with the abolition of the
top to bottom gradients in blood flow.
While mG would be expected to abolish apicobasal
differences in perfusion, it would not necessarily affect other nongravitational mechanisms of inhomogeneity. The persistence of cardiogenic oscillations in
mG implies that residual inhomogeneity persists in
the absence of gravity, and that these differences in
blood flow must be between widely separated regions
of the lung, since differences in blood flow on a very
small scale would not be expected to generate cardiogenic oscillations at the mouth.
Pulmonary Gas Exchange and Ventilation–
Perfusion Ratio
Resting V’ O2 and V’ CO2 are unchanged by exposure to
mG although there are some changes in the parameters associated with gas exchange. Tidal volume
is decreased by B15%, and there is a compensatory
increase in breathing frequency (9%). While the total
ventilation is decreased by B7%, when the reduction
in physiological deadspace resulting from the re’ is factored in, alveolar
moval of areas of high V’ A =Q
ventilation remains unchanged. The reasons for the
selection of a different combination of tidal volume
and breathing frequency are unclear. There was no
evidence of significant changes in respiratory drive.
Some flights have shown a small increase in end-tidal
PCO2 (B2.0 Torr), but since there were no changes in
end-tidal PO2 , this was probably due to the increased
environmental CO2 levels in the spacecraft.
There have been no direct measurements of ventilation–perfusion ratio distribution in mG. The
equipment needed for imaging techniques have not
been taken on space flights, and techniques such as
the multiple inert gas elimination technique (MIGET) are impractical. However, by performing a
controlled slow exhalation from TLC to RV following a period of air breathing the intrabreath respiratory exchange ratio can be calculated. Studies in
dogs challenged with methacholine have shown that
the slope of the intrabreath R plot with exhaled vol’ inequality
ume is correlated with the degree of V’ A =Q
determined by MIGET.
There were significant cardiogenic oscillations
seen in the CO2 expirogram in mG, which is strong
evidence for continued inter-regional differences in
’ There was also a marked reduction in V’ A =Q
’
V’ A =Q.
range after the onset of airways closure, consistent
with the idea that the top-to-bottom gradient in
’ had been abolished in mG. However, over
V’ A =Q
phase III of the prolonged expiration there was no
’ between standing and
change in the range of V’ A =Q
mG. This result was surprising given the prior observations that mG results in reduction in the topographical gradients of both ventilation and perfusion.
Thus, it appears that at lung volumes above the onset
of airways closure, the principal determinants of
’ inequality in normal subjects are not gravitaV’ A =Q
tional in origin, and there is some evidence to suggest
that gravity may actually impose some degree of
matching of ventilation to perfusion in the normal
lung.
Exercise
The ventilatory response to exercise is largely unaffected by mG. Maximum oxygen consumption seems
to be maintained in short-duration flights (9–14
days) suggesting no pulmonary limitation to exercise.
However, there is an abrupt reduction in peak V’ O2
upon return from short-duration space flight of
B22%. The V O2 response returns to preflight levels
within 6–9 days, with the recovery in the first 2 days
being extremely rapid, suggesting that adjustments
to the circulating blood volume of the subjects after
return are a major factor.
During short-duration flights, the cardiac output
increase with increasing V’ O2 is substantially lower
than that measured either upright or supine on the
ground preflight. No such data exist for long-duration space flight. The cause for these changes is unknown. Alterations in venous return that result from
mG may be a factor. If O2 delivery is controlled in
response to exercise, as opposed to cardiac output,
then the lower circulating blood volume in mG and
associated increase in [Hb] may result in lower cardiac output demands. Alternatively, sequestration
of circulatory blood volume in a more evenly filled
pulmonary circulation may be a factor. There may
also be changes in the efficiency of the muscle pump
returning blood to the thorax.
Ventilatory Control
Microgravity results in a substantial reduction in the
ventilatory response to hypoxia, but leaves the ventilatory response to CO2 essentially unchanged. The
hypercapnic response measured in the absence of any
hypoxic drive showed only a minor increase in the
118 SPACE, RESPIRATORY SYSTEM
slope of the rise in ventilation with CO2, with
changes in the break point such that ventilation at a
PCO2 of 60 mmHg was unchanged. In sharp contrast,
the isocapnic hypoxic ventilatory response (CO2
B46 mmHg) approximately halved in mG. There
was no change over the course of a 16-day flight,
suggesting the response was likely the result of a
mechanical change as opposed to some slower adaptation to mG. Importantly, the decrease in the
hypoxic response in mG was similar to that seen in
the same subjects when they were placed acutely into
the supine position in 1G. Simultaneous measurements of the inspiratory pressure measured 100 ms
after the unexpected occlusion of the inspiratory
path (an independent measure of ventilatory drive)
essentially mirrored the combined results of the
hypercapnic and hypoxic responses. This showed
that the changes were due to changes in the ventilatory response itself, and not the result of changes in
the mechanical configuration of the respiratory system limiting ventilation.
The likely cause of the change in the hypoxic response is an increase in blood pressure at the level of
the carotid bodies. While systemic blood pressure is
little changed by either the supine position or mG, in
the upright position in 1G, blood pressure at the carotid bodies is lower than at heart level due to the
hydrostatic pressure difference. This difference is
abolished in both the supine position and in mG.
Stimulation of the carotid baroreceptors results in an
inhibition of the carotid chemoreceptor output, and
this is thought to be the cause in this circumstance.
arousals per hour. Thus, mG significantly reduced
sleep-disordered breathing, probably because the
weight of the soft tissues of the pharynx is absent
in mG, eliminating their tendency to fall back and
obstruct the upper airway.
Inhaled Aerosols
Long-term space flight represents a situation in
which aerosol deposition may be an important health
consideration. The potential for significant airborne
particle loads is high since the environment is closed,
and no sedimentation occurs. Microgravity provides
for potentially high particle concentrations in the
periphery of the lung, since particles that normally
sediment will not be removed from the airways,
leaving them available for transport to the alveolar
regions.
There have been no studies of inhaled aerosols in
sustained mG to date but extensive studies have been
performed in parabolic flight. While total deposition
is greatly reduced in mG, there is an unexpectedly
high deposition of small particles (0.5–1 mm), with
this deposition being more peripheral. It seems that
with small particles, nongravitational factors such as
nonreversibility of flows, play a significant role in
determining particle deposition.
In future exploration missions, inhaled particles
may be a significant factor. The dust on the surface of
Mars is oxidative, due to the UV environment, and so
reacts in the presence of water. This combined with
the low gravity environment (B1/3G) may result in a
disproportionate response of the pulmonary system
to such dust.
Sleep
Sleep is reported to be poor in space flight. There are
numerous potential causes, especially in short-term
flights, including disruptions to circadian rhythms,
noise, and other environmental factors. At this time
the question of whether or not mG per se contributes
to sleep disruption remains unclear.
The record is however clearer with respect to
sleep-disordered breathing. Full polysomnography
performed on five subjects showed a significant reduction in the apnea-hypopnea index (AHI) from
8.3 h 1 preflight to 3.4 h 1 inflight, with one subject who showed mild sleep-disordered breathing
preflight having a reduction in AHI from 22.7 h 1 to
9.7 h 1 inflight. There were concomitant reductions
in the amount of time spent snoring. Preflight there
were on average 18 arousals per hour, 5.5 of which
could be attributed to respiratory events. Inflight, the
number of arousals fell to 13.4 h 1 almost entirely
as a consequence of a 70% reduction in the number
of respiratory-related arousals, which fell to only 1.8
Extravehicular Activity
Both the shuttle and the ISS have a 14.7 psia
(1013 kPa, 760 mmHg) 21% O2 environment. However, space suits operate at a very much lower pressure with a 100% O2 environment, in order to
maintain suit flexibility and, thus, astronaut mobility.
A direct transition from cabin pressure to suit pressure (US suit, 4.3 psia, B295 kPa, B220 mmHg; Russian suit, 5.9 psia, B405 kPa, B290 mmHg) would
result in decompression sickness (DCS). Therefore,
an extensive denitrogenation procedure must be performed before an extravehicular activity (EVA).
To date, no astronaut has formally reported DCS
during EVA, although at least one astronaut has
informally reported symptoms in the knee on two
occasions, Gemini X and Apollo 11, after depressurization to a 5.0 psia cabin pressure after several
hours of prelaunch O2 prebreathe. In contrast,
research subjects during prebreathe validation
tests report DCS in substantial numbers. There are
SPACE, RESPIRATORY SYSTEM 119
Figure 1 Astronaut Donald Petit performing a pulmonary function experiment on board the US International Space Station in 2003. He
is holding a breathing assembly in his right hand. Flows are measured by a pneumotachograph (blue component of the breathing
assembly) and gas concentrations are measured by a mass spectrometer mounted in the rack in front of him. In his left hand is a large
pneumotachograph for performing maximum expiratory flow-volume curves. Photo courtesy of NASA.
numerous reasons why DCS may not have been
reported in EVA including the routine use of analgesics prior to EVA, masking of joint symptoms
while working in uncomfortable space suits, repressurization at the completion of the EVA, and underreporting by the flight crew.
It is however almost certain that venous gas emboli
(VGE) are present in EVA. In a study of comparable
prebreathes and decompressions to those used during
EVA, more than 50% of the participants had detectable bubbles as indicated by Doppler ultrasound.
The lungs act as a filter for the bubbles. During ascents from deep saturation dives these bubbles have
’
been shown to significantly alter the range of V’ A =Q
in the lung as evidenced by the intrabreath measure’ presumably as a result of their emments of V’ A =Q,
bolic effects. In a recent study on the ISS, astronauts
’ inperforming EVA measured the degree of V’ A =Q
equality before and on the day following EVA. There
’
was no significant change in the degree of V’ A =Q
inequality in the lungs of the crew members 24 h after EVA, suggesting that the current denitrogenation
protocols are sufficiently protective to not cause
long-term harm to the lungs of the EVA crew.
Whether or not there is an acute effect of VGE
resulting from EVA remains unknown.
Respiratory Diseases in Space Flight
Essentially nothing is known about pulmonary diseases in space flight. While it is clear that some
pulmonary diseases, for example, pneumonia and
tuberculosis, have significant gravitational components, there are no reports of such problems in space
flight. The population that flies is typically in their
lower middle-age, healthy, and of above average fitness; a circumstance that is unlikely to change until
space flight becomes much more accessible than is
currently the case (Figure 1).
See also: Aerosols. Chemoreceptors: Central; Arterial.
Diving. Environmental Pollutants: Overview; Particulate Matter, Ultrafine Particles. Exercise Physiology.
Fluid Balance in the Lung. High Altitude, Physiology
and Diseases. Hyperbaric Oxygen Therapy. Oxygen
Toxicity. Particle Deposition in the Lung. Peripheral Gas Exchange. Pulmonary Circulation. Sleep
Apnea: Overview. Sleep Disorders: Overview. Ventilation: Control.
Further Reading
Estenne M, Paiva M, and Engel LA (1995) Gravity. In: Roussos C
(ed.) The Thorax, pp. 1515–1539. New York: Dekker.
Paiva M and Engel LA (1989) Gas mixing in the lung periphery. In:
Chang HK and Paiva M (eds.) Respiratory Physiology (Lung
Biology in Health and Disease Series), vol. 40, pp. 245–276.
New York: Dekker.
Prisk GK (2000) Invited review: microgravity and the lung. Journal
of Applied Physiology 89: 385–396.
Prisk GK, Paiva M, and West JB (2001) Gravity and the Lung:
Lessons from Microgravity. New York: Dekker.
West JB (1992) Life in space. Journal of Applied Physiology 72:
1623–1630.
West JB, Elliott AR, Guy HJB, and Prisk GK (1997) Pulmonary
function in space. JAMA 277: 1957–1961.
West JB, Guy HJB, Elliott AR, and Prisk GK (1996) Respiratory system in microgravity. In: Fregly MJ and Blatteis
CM (eds.) The Handbook of Physiology Section 4: Environmental Physiology, pp. 675–689. New York: Oxford University
Press.