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Adaptation to Acceleration Environments

Russell R. Burton, Arthur H. Smith

10.1002/cphy.cp040240

Source: Supplement 14: Handbook of Physiology, Environmental Physiology

Originally published: 1996

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Physics of Acceleration
1.1 Interaction of Forces and Mass
1.2 Acceleration of Circular Motion (Physics of the Centrifuge)
1.3 Acceleration without Inducing Weight
1.4 Acceleration of Aircraft
1.5 Acceleration of Rockets
2 Research Centrifuges
2.1 Sustained‐G Centrifuges
2.2 Chronic‐G Centrifuges
3 Acceleration Nomenclature
4 Sustained G
4.1 High Sustained G (HSG)
4.2 Cardiovascular Accommodation to +Gz
4.3 Neurologic Accommodation to +Gz
4.4 Lung and Respiration Accommodation to +Gz
4.5 Physiological Accommodation to ‐Gz ±Gx and +Gy
4.6 G Tolerances
4.7 Adaptation to Sustained G
4.8 Cross Adaptation
4.9 Natural Bases for Sustained‐G Homeostasis
5 Chronic G
5.1 Adaptation Process
5.2 Structural and Functional Changes
5.3 Adaptation to Hypo‐ and Hypergravity Fields
5.4 Utilization of Gravitational G in Space
6 Conclusion
Figure 1. Figure 1.

Diagram showing physics of acceleration, r, radius of rotation (cm); V, rate of motion (cm/s; velocity); a, acceleration (dynes; centripetal) force; Gc inertial (dynes; centrifugal) force; g, Earth's gravitational constant (980 dynes); GR, resultant G vector.
Figure 2. Figure 2.

Methods of providing a weightless or microgravity environment.
Figure 3. Figure 3.

Eye‐level Pa analog recording of a human exposed to +3.2 Gz for 9 s on the left and exhibiting insufficient cardiovascular recovery. Grayout (peripheral light loss) occurred that would have been quickly followed with loss of consciousness if the centrifuge had not been stopped. The recording of +3 Gz on the right shows adequate cardiovascular recovery.
Figure 4. Figure 4.

Measured G‐level tolerances of the human compared with a curve derived from Eq. 2 23.
Figure 5. Figure 5.

The reduction in carotid arterial pressure (Pa) during +Gz exposure is integrated, correlated with the +Gz area, and compared for the dog, nonhuman primate, and the human

Modified from Pertzoff and Britton 126
Figure 6. Figure 6.

Direct eye‐level arterial blood pressure and esophageal pressure (a measure of pulmonary pressure) changes during +Gz of a subject while performing an AGSM. Mean Pa falls to near zero during the inspiratory phase.
Figure 7. Figure 7.

Relationship between the abdominal venous pressure (AVP)–central venous pressure (CVP) gradient, and venous flow (L/min) found in swine before (control) and during the 3, 5, and 7 + Gz levels, with and without AGSM. Data are shown with (WS) and without (W/OS) G‐suit inflation. Circled numbers are data at that +Gz level WS. Regression equation includes control plus no strain data.

From Burns et al. 20 with permission
Figure 8. Figure 8.

Relative (%) volume changes in the pelvis (abdominal region), thigh, and calf of the human during onset of G with and without the anti‐G suit. Volume increases are represented with changes in electrical resistance using an impedance plethysmograph.
Figure 9. Figure 9.

The maintenance of a constant arterio–venous pressure differential is shown as the arterial pressure becomes subatmospheric at head level.

Adapted from Henry et al. 72 with permission
Figure 10. Figure 10.

Oxygen and CO2 pressure gradients between alveoli (PA) and Pulmonary blood (Pa) as a function of increasing G.

Data from Burton et al. 30
Figure 11. Figure 11.

The effect of various levels of ‐Gz on group mean heart rates.

Modified from Ryan et al. 135
Figure 12. Figure 12.

Relationship between cerebrospinal fluid (CSF) pressure and venous pressure (Pv) (cm) during positive and negative radial accelerations of varying magnitudes. Increased pressures occurred under negative G.

Modified from Rushmer et al. 134
Figure 13. Figure 13.

Arterial oxygen saturations measured in subjects during exposure to ±6 Gx for 1 min.

Modified from Smedal et al. 146
Figure 14. Figure 14.

Tolerance of rats exposed to positive +Gz acceleration. Curves delineate 100% survival and 100% mortality.

Modified from Cranmore 45
Figure 15. Figure 15.

Acceleration tolerance curves for humans and monkeys. Unconsciousness end points were used for both species.

Modified from Kydd and Stoll 97
Figure 16. Figure 16.

Human tolerance times (min) at different +Gz levels using fatigue as the end point. Number of subjects is in parentheses.

Modified from Burton 26; data from Miller et al. 109
Figure 17. Figure 17.

Survival of rats at +20 Gz with prior repeated acceleration exposures of +2 Gz (closed circles) and +12 Gz (open triangles) and controls with no prior acceleration exposure.

Modified from Frazer and Reeves 57
Figure 18. Figure 18.

Effect of duration of acceleration on extensive:flexor muscle ratios. Rates of change (with time [t] in months) in the mass ratios of adductor (E) and sartorius (F) muscles have the kinetics:Data for 0G represents intercept values from observations at several fields at the exposure times indicated.

From Burton et al. 28
Figure 19. Figure 19.

Influence of the ambient acceleration field on mature body mass of chickens. Mature body mass (M) of chronically accelerated chickens decreases rectilinearly with increasing field strength G:where M is mature body mass (kg), G is a field of G‐strength, M0 is weighlessness; i.e., G = 0; and, ‐k is the proportionality coefficient. For the indicated observations 151, the constants in the above equation have the values: M0 = 2.13 kg and ‐k = ‐0.17; with a correlation coefficient r = 0.63 (P < 0.01).

From Smith and Burton 151


Figure 1.

Diagram showing physics of acceleration, r, radius of rotation (cm); V, rate of motion (cm/s; velocity); a, acceleration (dynes; centripetal) force; Gc inertial (dynes; centrifugal) force; g, Earth's gravitational constant (980 dynes); GR, resultant G vector.



Figure 2.

Methods of providing a weightless or microgravity environment.



Figure 3.

Eye‐level Pa analog recording of a human exposed to +3.2 Gz for 9 s on the left and exhibiting insufficient cardiovascular recovery. Grayout (peripheral light loss) occurred that would have been quickly followed with loss of consciousness if the centrifuge had not been stopped. The recording of +3 Gz on the right shows adequate cardiovascular recovery.



Figure 4.

Measured G‐level tolerances of the human compared with a curve derived from Eq. 2 23.



Figure 5.

The reduction in carotid arterial pressure (Pa) during +Gz exposure is integrated, correlated with the +Gz area, and compared for the dog, nonhuman primate, and the human

Modified from Pertzoff and Britton 126


Figure 6.

Direct eye‐level arterial blood pressure and esophageal pressure (a measure of pulmonary pressure) changes during +Gz of a subject while performing an AGSM. Mean Pa falls to near zero during the inspiratory phase.



Figure 7.

Relationship between the abdominal venous pressure (AVP)–central venous pressure (CVP) gradient, and venous flow (L/min) found in swine before (control) and during the 3, 5, and 7 + Gz levels, with and without AGSM. Data are shown with (WS) and without (W/OS) G‐suit inflation. Circled numbers are data at that +Gz level WS. Regression equation includes control plus no strain data.

From Burns et al. 20 with permission


Figure 8.

Relative (%) volume changes in the pelvis (abdominal region), thigh, and calf of the human during onset of G with and without the anti‐G suit. Volume increases are represented with changes in electrical resistance using an impedance plethysmograph.



Figure 9.

The maintenance of a constant arterio–venous pressure differential is shown as the arterial pressure becomes subatmospheric at head level.

Adapted from Henry et al. 72 with permission


Figure 10.

Oxygen and CO2 pressure gradients between alveoli (PA) and Pulmonary blood (Pa) as a function of increasing G.

Data from Burton et al. 30


Figure 11.

The effect of various levels of ‐Gz on group mean heart rates.

Modified from Ryan et al. 135


Figure 12.

Relationship between cerebrospinal fluid (CSF) pressure and venous pressure (Pv) (cm) during positive and negative radial accelerations of varying magnitudes. Increased pressures occurred under negative G.

Modified from Rushmer et al. 134


Figure 13.

Arterial oxygen saturations measured in subjects during exposure to ±6 Gx for 1 min.

Modified from Smedal et al. 146


Figure 14.

Tolerance of rats exposed to positive +Gz acceleration. Curves delineate 100% survival and 100% mortality.

Modified from Cranmore 45


Figure 15.

Acceleration tolerance curves for humans and monkeys. Unconsciousness end points were used for both species.

Modified from Kydd and Stoll 97


Figure 16.

Human tolerance times (min) at different +Gz levels using fatigue as the end point. Number of subjects is in parentheses.

Modified from Burton 26; data from Miller et al. 109


Figure 17.

Survival of rats at +20 Gz with prior repeated acceleration exposures of +2 Gz (closed circles) and +12 Gz (open triangles) and controls with no prior acceleration exposure.

Modified from Frazer and Reeves 57


Figure 18.

Effect of duration of acceleration on extensive:flexor muscle ratios. Rates of change (with time [t] in months) in the mass ratios of adductor (E) and sartorius (F) muscles have the kinetics:Data for 0G represents intercept values from observations at several fields at the exposure times indicated.

From Burton et al. 28


Figure 19.

Influence of the ambient acceleration field on mature body mass of chickens. Mature body mass (M) of chronically accelerated chickens decreases rectilinearly with increasing field strength G:where M is mature body mass (kg), G is a field of G‐strength, M0 is weighlessness; i.e., G = 0; and, ‐k is the proportionality coefficient. For the indicated observations 151, the constants in the above equation have the values: M0 = 2.13 kg and ‐k = ‐0.17; with a correlation coefficient r = 0.63 (P < 0.01).

From Smith and Burton 151
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Article Title: Adaptation to Acceleration Environments
 

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Russell R. Burton, Arthur H. Smith. Adaptation to Acceleration Environments. Compr Physiol 2011, Supplement 14: Handbook of Physiology, Environmental Physiology: 943-970. First published in print 1996. doi: 10.1002/cphy.cp040240