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Full text of "Physiology of prolonged bed rest"

NASA Technical Memorandum 101010 

NASA-TM-101010 19880019223 



Physiology of Prolonged 
Bed Rest 

J. E. Greenleaf 



August 1988 StP ^. i980 

LA.'j-.iiiiv r;;:.-!"ARCH CEru'r? 



fU/NSA 

National Aeronautics and 
Space Administration 



NASA Technical Memorandum 101010 



Physiology of Prolonged 
Bed Rest 

J. E. Greenleaf, Ames Research Center, Moffett Field, California 



August 1988 



rVI/NSA 

National Aeronautics and 
Space Administrafion 

Ames Research Center 

Moffett Reld, California 94035 



//2?-Z?d.a7 



^ 



PHYSIOLOGY OF PROLONGED BED REST 

J E Greenleaf 

Laboratory for Human Environmental Physiology 
Space Physiology Branch, NASA Ames Research Center 
Moffett Field, California 94035 U.S.A. 



ABSTRACT 

Rest in bed has been a normal procedure used by physicians for centuries in the 
treatment of injury and disease. Exposure of patients to prolonged bed rest 
(>24 hr) in the horizontal position induces adaptive deconditioning responses. 
Thus "healing" proceeds concomitantly with deconditioning. While deconditioning 
responses are appropriate for patients or test subjects in the horizontal posi- 
tion, they usually result in adverse physiological responses, such as fainting and 
muscular weakness, when the patients assume the upright posture. These decondi- 
tioning responses result from reduction in hydrostatic pressure within the cardio- 
vascular system, virtual elimination of longitudinal pressure on the long bones, 
some decrease in total-body metabolism (exercise), changes in diet, and perhaps 
psychological impact from the different environment. Essentially every system in 
the body is affected by bed-rest deconditioning. An early stimulus is the 
cephalic shift of fluid from the legs which increases atrial pressure and induces 
compensatory responses for fluid and electrolyte redistribution. Without counter- 
measures, deterioration in strength and muscle function occurs within 1 wk while 
increased calcium loss may continue for months. In addition to problems with the 
cardiovascular, muscle and bone systems, increased research efforts should be 
focused on the effects of deconditioning on drug and carbohydrate metabolism, and 
the immune system. 



KEYWORDS 

Bed-rest deconditioning, remedial exercise training, fluid-electrolyte metabolism, 
hydrostatic pressure, carbohydrate metabolism.* 



INTRODUCTION 

Prolonged bed rest has been used by physicians for centuries in treating illness 
and injury. Some infirmities may require rest for the patient, but the recumbent 
position may not be necessary. Other infirmities may have required that the 



patient should not stand, but there was no reason to reduce or eliminate physical 
exercise. The deconditioning (acclimation) responses of healthy and sick or 
injured patients subjected to bed rest are caused by some combination of reduction 
of hydrostatic pressure within the cardiovascular system, greatly reduced pressure 
on the long bones, probable reduction in exercise metabolism, dietary changes, and 
probably changed psychological inputs from the different environment. Thus, early 
in bed rest, the healing process occurs simultaneously with the deconditioning 
syndrome. It is unknown whether deconditioning helps or hinders healing. 

Asher (1947) has described vividly the major factors contributing to the decondi- 
tioning process: "Look at a patient lying long in bed, what a pathetic picture he 
makes! The blood clotting in his veins, the lime draining from his bones, the 
scybala stacking up in his colon, the flesh rotting from his seat, the urine leak- 
ing from his distended bladder, and the spirit evaporating from his soul!" 

The mechanisms of this bed-rest deconditioning syndrome have only just begun to be 
studied in detail. The first step was to collate the signs, symptoms, and physio- 
logical changes and organize them into a time distribution. Table 1. From this 
table it is clear that fluid-electrolyte parameters are disturbed early in bed 
rest; muscle atrophy next (increased urine nitrogen and hydroxyproline; reduced 
lean body mass); and significant urine calcium loss and decreased bone density 
occur later. 



FLUID-ELECTROLYTE SHIFTS 

To simulate the physiological responses of astronauts during exposure to micro- 
gravity (weightlessness), the head-down posture (by S'-S" from horizontal) has 
been adopted. With head-down bed rest the same changes occur as during horizontal 
bed rest, but they happen more quickly. Initially, when the body is moved from 
the sitting or standing position to the slightly head-down position, fluid shifts 
from the extremities (mainly thighs and legs) to the thorax and head resulting in 
various signs and symptoms, some inducing discomfort (Table 2). Most disappear by 
the fourth day. Fifteen minutes after head-down tilt this headward fluid shift 
increased stroke volume and central venous pressure (from 9 to 13 cm H2O, 
P < 0.05) with no change in heart rate and a decrease in total peripheral resis- 
tance (Gaffney, 1985). Four hours after -5' head-down tilt the interstitial fluid 
pressures (measured with wick catheters) decreased from 4.6 to -2.8 mmHg 
(P < 0.05) in the anterior tibialis and from 0.6 to -3.8 mmHg (P < 0.05) in leg 
subcutaneous tissue (Hargens, 1983) suggesting tissue to vascular space fluid 
shifts. About 900 ml of fluid shifts from the two thighs and legs. Plasma volume 
increases by 11.5% after 30 min of tilt and then decreases by 125 ml (4%) at 6 hr, 
by 150-300 ml (5-10?) after 24 hr, by 350-450 ml (10-13?) on day 4, and can reach 
-30? at 180 days of bed rest (Donaldson, 1969; Gauquelin, 1985; Nixon, 1979; 
Volicer, 1976; Fig. 1). These plasma volume losses are not influenced by moderate 
isotonic or isometric exercise training during bed rest (Greenleaf, 1977b); but 
heavy isotonic training can maintain plasma volume at control levels during one 
month of -6" bed rest (Greenleaf, 1988). The decrease in body water during the 
first 24 hr of bed rest occurs via an osmotic diuresis (V = 2.5 ml/min) followed 
by a small increase in urine output (1.5 to 2.0 ml/min) during 7-14 days; volun- 
tary fluid intake is unchanged (Greenleaf, 1977a). The initial stimulus for the 
diuresis appears to be the increase in central venous pressure that is associated 



TABLE 1 . Physiological changes during bed rest 



0-3 Days 



4-7 Days 



8-14 Days 



Over 15 days 



Increases in: 



Increases in: 



Increases in: 



Increases m: 



Urine volume 
Urine Na*, CI", 

Ca and osmoi 

excretion 
Plasma osmolality 
Hematocrit 
Venous compliance 

Decreases in : 

Total fluid intake 
Extracellular 

(plasma, 

interstitial) 

and intracellular 

volumes 
Calf blood flow 
Resting heart rate 
Secretion of 

gastric Juice 
Glucose tolerance 
Head-to-foot C+G^) 

acceleration 

tolerance 



Urine creatinine, 
hydroxyproline, 
phosphate, nitro- 
gen, and potassium 
excretion 

Plasma globulin, 
phosphate and 
glucose 
concentrations 

Blood fibrinogen 

Fibrinolytic 
activity and 
clotting time 

Focal point 

Hyperemia of eye 
conjunctiva and 
dilation of 
retinal arteries 
and veins 

Auditory threshold 

Decreases in : 

Near point of 

visual acuity 
Orthostatic 

tolerance 
Nitrogen balance 



Urine pyrophosphate 
Sweating 

sensitivity 
Exercise 

hyperthermia 
Exercise maximal 

heart rate 

Decreases in : 

Red blood cell mass 
Leucocyte 

phagocytosis 
Tissue heat 

conductance 
Lean body mass 
Body fat content 



Peak hypercaiciuria 
Sensitivity to 

thermal stimuli 
Auditory threshold 

(secondary) 

Decreases in : 
Bone density 



with moderate decreases in plasma aldosterone, renin activity, and vasopressin 
which return to normal after 24 hr (Nixon, 1979). The general consensus is that 
neither renal plasma flow, glc"ierular filtration rate, nor the functioning of the 
adrenergic nervous system (plasma catecholamines) are changed during bed rest 
(Chobanian, 1974; Fuller, 1970; Pequignot, 1985; Zager, 1974). Gharib (1985) 
reported a slight, transient increase in plasma atrial natriuretic factor during 
the first 30 rain of -9° bed rest that would have been too short a response to 
account for the Na-osmotic diuresis on the first day of bed rest. Because cardiac 
transplant patients exhibit diuretic responses, although somewhat attenuated, to 
water immersion (Convertino, 1984), clearly redundant mechanisms that are not 
fully inderstood must be available to control fluid-electrolyte metabolism during 
bed rest. 



TABLE 2. Time course of signs and symptoms causing discomfort in men during -6° 

head-down bed rest (Giiell et ai. 1984). 



Symptomatology Subjects Beginning, Maximum, Disappearance, 

hours hours hours 



Feeling of head fullness 


3 


2 


12 


24 


Masai congestion 


3 


4 


24 


96 


Buccal and gingival turgescenoe 


3 


4-6 


48 


96 


Facial oedema 


3 


24 


48 


72 


Palpebral oedema 


3 


24 


48 


96 


Headache 


1 


24 


48 


72 


Dizziness 


1 


~ 


48 


~ 



LEAN BODY MASS 

Lean body mass (LBM) comprises everything in the body besides fat. Thus it 
involves mainly water, muscle, and bone. Regarding muscle, calf circumferences 
and lower leg volumes were decreased significantly by 3.3!i and ^.5%, respectively, 
after 8 hr of -5° bed rest; but soleus muscle water content was unchanged while 
fluid continued to be lost from the anterior tibialis and overlying subcutaneous 
tissue (Hargens, 1983). These small decreases in muscle water content caused no 
significant change in plantar flexion isometric or isokinetic peak torque 
strengths. With an adequate diet (2,800-3,100 kcal/day), there are minimal 
changes in LBM. Total LBM decreases by about 0.8 kg after 14 days of horizontal 
bed rest without exercise training, by 1.1 kg with isometric training, and by 
1.0 kg with isotonic training (Greenleaf, 1977a). Corresponding losses in body 
fat were 0.2 kg, 0.2 kg, and 0.7 kg, respectively. Thus, loss of body fat content 
is proportional to total metabolism while loss of LBM appears to be associated 
with the reduced hydrostatic pressure. Results from a more recent study indicated 
no significant changes in peak O2 uptake, strength, and endurance in healthy men 
after 30 days of -6° bed rest with performance of daily, strenuous isokinetic and 
isotonic exercise training (Greenleaf, unpublished data). So reduced aerobic 
working capacity, muscular strength, and endurance are not inevitable consequences 
of exposure to prolonged bed rest. Body density was unchanged in the exercise 
group and also in the nonexercise group. So moderate activity (movement) during 
bed rest in healthy men without additional exercise training can essentially pre- 
serve muscular strength, but not aerobic capacity. 

Nitrogen balance becomes negative for the first 60-90 days of bed rest and then 
returns to essentially zero (reaches equilibrium) after 182-252 days of bed rest; 
exercise during bed rest accentuates nitrogen loss (Bychkov, 1979, Donaldson, 
1969). 

Like aging, bed-rest deconditioning results in loss of bone mineral content (BMC) 
and total body calcium. The latter decreases by about 6.1 mg/day over 35 days of 
bed rest, and the decrease is reduced to 0.9-1.1 mg/day over 140 to 252 days of 
bed rest (Donaldson, 1970; Greenleaf, 1977a; LeBlanc, 1987; Lynch, 1967; 



-6 



-12 



CO 

t/i 

O 

-I 

UJ 

S 

= -15 

O 

> 
< 

I -18 

< 



-21 



-24 



-27 - 



-30 l- 



PV LOSS - BR DAYS/-0.011 + (-0.0013)(BR DAYS) 




80 100 120 140 

BED REST (days) 



160 



180 



200 



220 



FIG. 1. Plasma volume loss during bed rest with data from studies that used no 
remedial procedures (from Greenleaf et al., 1977b, with permission). 



Schneider, 1984; Whedon, 1949). The change appears to follow a logarithmic decay 
curve; the rate of Ca loss decreases as bed rest lengthens. Because vigorous 
exercise training during bed rest has no effect on the rate of urinary Ca loss 
(Greenleaf, 1977a; Rodahl, 1967), the hypercalciuria could be the result of 
reduced hydrostatic pressure; i.e., change in bone blood flow and/or to the large 
reduction in axial pressure on the skeleton. Whedon (1949) found that fluid 
shifting and axial loading in an oscillating bed (+0^ to -G^) during bed rest 
reduced hypercalciuria by 51/5. Also, quiet standing for 3 hr/day during bed rest 
significantly reduces urinary Ca loss (Issekutz, 1966). Standing increases bone 
axial pressure and hydrostatic pressure. Thus, increasing axial pressure, perhaps 
by impact loading, would be a most appropriate remedial procedure to attenuate 
bed-rest-induced hypercalciuria. 

The basic premise is that increased excretory Ca loss during bed rest will induce 
reduction in bone mineral content. Bone mineral content of the lumbar spine and 
radius is unchanged in nonexercised and exercise-trained men after 4 weeks of -6' 
bed rest (Arnaud, 1987), and in nonexercised men during 5 weeks of horizontal bed 



rest (LeBlanc, 1987). Further, there is no change in iliac crest biopsy param- 
eters (trabecular volume, mean cortical thickness, or mean trabecular plate thick- 
ness) in nonexercise or exercise-trained men after 120 days of -5' bed rest (Vico, 
1987). Thus, the rather meager evidence suggests that bone mineral content (den- 
sity) is not significantly reduced in healthy men over 4 months of bed rest. 



REFERENCES 

Arnaud, S., Berry, P., Cohen, M., Danellis, J., DeRoshia, C, Greenleaf, J., 
Harris, B., Keil, L., Bernauer, E., Bond, M., Ellis, S., Lee, P., 
Selzer, R., and Wade, C. (1987): Exercise countermeasures for bed rest 
deconditioning. Washington, D.C.: NASA Space Life Sciences Symp .. 59-60. 

Asher, R.A.J. (1947): The dangers of going to bed. Brit. Med. J . U, 967-968. 

Bychkov, V.P., Borodulina, I.I., and Sivuk, A.K. (1979): Distinctions referable 
to excretion of end products of protein metabolism in urine of man sub- 
mitted to 182-day antiorthostatic hypokinesia. Kosm. Biol. Aviakosm. Med . 
13, 39-42. 

Chobanian, A.V., Lille, R.D., Tercyak, A., and Blevins, P. (1974): The metabolic 
and hemodynamic effects of a prolonged bed rest in normal subjects. 
Circulation 49, 551-559. 

Convertino, V.A., Benjamin, B.A., Keil, L.C., and Sandler, H. (1984): Role of 
cardiac volume receptors in the control of ADH release during acute simu- 
lated weightlessness in man. Physiologist 27, S51-S52. 

Donaldson, C.L,, Hulley, S.B., McMillan, D.E., Hattner, R.S., and Bayers, J.H. 

(1969): The effect of prolonged simulated nongravitational environment on 
mineral balance in the adult male. NASA CR-108314, 1-91. 

Fuller, J.H., Bernauer, E.M., and Adams, W.C. (1970): Renal function, water and 
electrolyte exchange during bed rest with daily exercise. Aerospace Med . 
41, 60-72. 

Gaffney, F.A., Nixon, J.V., Karlsson, E.S., Campbell, W., Dowdey, A. B.C., and 

Blomqvist, C.G. (1985): Cardiovascular deconditioning produced by 20 hours 
of bedrest with head-down tilt (-5°) in middle-aged healthy men. Am. J. 
Cardiol . 56, 634-638. 

Gauquelin, G., Guell, A., Mauroux, J.L., Geelen, G., Annat, G., Vincent, M., 
Allevard, A.M., Sassolas, A., Bizollon, C.A., and Gharib, C. (1985): 
Volume regulating hormones during a 5-hour head-down tilt at -10°: II - 
plasma renin activity and aldosterone. ESA SP-237, 191-193. 

Gharib, C, Gauquelin, G., Geelen, G., Cantin, M., Gutovska, J., Mauroux, J.L., 
and Giiell, A. (1985): Volume regulating hormones (renin, aldosterone, 
vasopressin and natriuretic factor) during simulated weightlessness. 
Physiologist 28, S30-S33. 

Greenleaf, J.E., Bernauer, E.M. , Juhos, L.T., Young, H.L., Morse, J.T., and 

Staley, R.W. (1977a): Effects of exercise on fluid exchange and body com- 
position in man during 14-day bed rest. J. Appl. Phvsiol . 43, 126-132. 

Greenleaf, J.E., Bernauer, E.M., Young, H.L., Morse, J.T., Staley, R.W., Juhos, 
L.T., and Van Beaumont, W. (1977b): Fluid and electrolyte shifts during 
bed rest with isometric and isotonic exercise. J. Appl. Physiol . 42, 
59-66. 

Greenleaf, J.E., Wade, C.E., and Leftheriotis, G. (1988): Orthostatic responses 
following 30-day bed rest deconditioning with isotonic and isokinetic exer- 
cise training. Aviat. Space Environ. Med ., 1989, in press. 



Giiell, A,, Pourcelot, L., Mauroux, J.L., Dupui, Ph., and Bes, A. (1984): Interest 
of head-down tilt to simulate the neurocirculatory modifications observed 
during space flight. Proc. 35th Cong. Int. Astro. Fed . IAF-84-190, 1-4. 

Hargens, A.R., Tipton, CM., Gollnick, P.D., Mubarak, S.J., Tucker, B.J., and 
Akeson, W.H. (1983): Fluid shifts and muscle function in humans during 
acute simulated weightlessness. J. Appl. Physiol . 54, 1003-1009. 

Issekutz, B., Jr., Blizzard, J.J., Birkhead, N.C., and Rodahl, K. (1966): Effect 
of prolonged bed rest on urinary calcium output. J. AddI. Physiol . 21, 
1013-1020. 

LeBlanc, A., Schneider, V., Krebs, J., Evans, H., Jhingran, S., and Johnson, P. 
(1987): Spinal bone mineral after 5 weeks of bed rest. Calcif. Tissue 
Int. 41, 259-261. 

Lynch, T.N., Jensen, R.L., Stevens, P.M., Johnson, R.L., and Lamb, L.E. (1967): 
Metabolic effects of prolonged bed rest: their modification by simulated 
altitude. Aerospace Med . 38, 10-20. 

Mixon, J. v., Murray, R.G., Bryant, C, Johnson, R.L., Mitchell, J.H., Holland, 
O.B., Gomez-Sanchez, C., Vergne-Marini, P., and Blomqvist, C.G. (1979): 
Early cardiovascular adaptation to simulated zero gravity. J. Aopl. 
Physiol . 46, 541-548. 

Pequignot, J.M., Giiell, A., Gauquelin, G., Jarsaillon, E., Annat, G., Bes, A., 

Peyrin, L., and Gharib, C. (1985): Epinephrine, norepinephrine, and dopa- 
mine during a 4-day head-down bed rest. J. Appl. Physiol . 58, 157-163. 

Rodahl, K., Birkead, N.C., Blizzard, J.J., Issekutz, B., Jr., and Pruett, E.D.R. 

(1967): Physiological changes during prolonged bed rest. In Nutrition and 
Physical Activity , ed. G. Blix, pp. 107-113. Uppsala: Almqvist and 
Wiksells, Inc. 

Schneider, V.S., and McDonald, J. (1984): Skeletal calcium homeostasis and coun- 
termeasures to prevent disease osteoporosis. Calcif. Tissue Int . 36, 
S151-S154. 

Vico, L., Chappard, D., Alexandre, C, Palle, S., Minaire, P., Riffat, G., 

Morukov, B., and Rakhmanov, S. (1987): Effects of a 120 day period of bed- 
rest on bone mass and bone cell activities in man: attempts at countermea- 
sures. Bone & Mineral 2, 383-394. 

Volicer, L., Jean-Charles, R., and Chobanian, A.V. (1976): Effect of head-down 
tilt on fluid and electrolyte balance. Aviat. Space Environ. Med . 47, 
1065-1068. 

Whedon, G.D., Deitrick, J.E., and Shorr, E. (1949): Modification of the effects 

of immobilization upon metabolic and physiologic functions of normal men by 
the use of an oscillating bed. Am. J. Med . 6, 684-711. 

Zager, P.G., Melada, G.A., Goldman, R.H., Gonzales, CM., and Luetscher, J. A. 

(1974): Increased plasma renin activity (PRA) in prolonged bedrest. vL 
Clin. Endocrinol . 53f 87a. 



Gueil, A., Pourceioc, 1., Mauroux, J.L., Dupui. Ph., ana 3es, A. (1984): Interesc 
of head-down cilt to simulate the neurocircuiacory modificacions observed 
during space flight. Proc. 35th Cong. Int. Astro. Fed . IAF-34-190, 1-^. 

Hargens, A.R., Tipton, CM., Gollnick, P.O., Mubarak, 3. J., Tucker, 3. J., and 
Akeson, W.H. (1983): Fluid shifts and muscle funccion in humans during 
acute simulated weightlessness. J. Appl. Physiol . 54, 1003-1009. 

Issekutz, 3., Jr., Blizzard, J.J., Birkhead, N.C., ana Rodahl, K. (1966): Effect 
of prolonged bed rest on urinary calcium output. J. Appl. Phvsiol . 21, 
1G13-'02O. 

LeBlanc, A., Schneider, V., Xrebs, J., Evans, H. , Jhingran, S., and Johnson. P. 
(1987): Spinal bone mineral after 5 weeks of bed rest. Calcif. Tissue 
Int . 41, 259-261. 

Lynch, T.N., Jensen, R.L., Stevens, P.M., Johnson, R.L., and Lamb, L.E. (1967): 
Metabolic effects of prolonged bed rest: their modification by simulated 
altitude. Aerospace Med . 38, 10-cO. 

Mixon, J. v., Murray, R.G., Bryant, C., Johnson, R.L., Mitchell, J.H., Holland, 
O.B., Gomez-Sanchez, C., Vergne-Marini, P., and Blomqvist, C.G. (1979): 
Early cardiovascular adaptation to simulated zero gravity. J . AddI . 
Phvsiol . 46, 541-548. 

Pequignot, J.M., Guell, A., Gauquelin, G., Jarsailion, E., Annat, G., Bes, A., 

Peyrin, L., and Gharib, C. (1985): Epinephrine, norepinephrine, and dopa- 
mine during a 4-day head-down bed rest. J. Appl. Physiol . 58, 157-163. 

Rodahl, K., Birkead, N.C., Blizzard, J.J., Issekutz, B., Jr., and Pruett, E.D.H. 

(1967): Physiological changes during prolonged bed rest. In Mutrition and 
Physical Activity , ed. G. Blix, pp. 107-113. Uppsala: Almqvist and 
Wiksells, Inc. 

Schneider, V.S., and McDonald, J. (1984): Skeletal calcium homeostasis and coun- 
terraeasures to prevent disease osteoporosis. Calcif. Tissue Int . 36, 
SI51-SI54. 

Vico, L., Chappard, D., Alexandre, C, Palle, S., Minaire, P., Riff at, G., 

Morukov, B., and Rakhmanov, S. (1987): Effects of a 120 day period of bed- 
rest on bone mass and bone cell activities in man: attempts at countermea- 
sures. Bone 4 Mineral 2, 383-394. 

Volicer, L., Jean-Charles, R., and Chobanian, A.V. (1976): Effect of head-down 
tilt on fluid and electrolyte balance. Aviat. Space Environ. Med . 47, 
1065-1068. 

Whedon, G.D., Deitrick, J.E., and Shorr, E. (1949): Modification of the effects 

of immobilization upon metabolic and physiologic functions of normal men by 
the use of an oscillating bed. Am. J. Med . 6, 684-711. 

Zager, P.G., Melada, G.A., Goldman, R.H., Gonzales, CM., and Luetscher, J. A. 

(1974): Increased plasma renin activity (PRA) in prolonged bedrest. J. 
Clin. Endocrinol. 53, 87a. 



rVIASA 

^■'(MCt' AcJtTiiniSlMlion 



Report Documentation Page 



1. Report No. 
NASA TM-101010 



2. Government Accession No. 



3. Recipient's Catalog No. 



4. Title and Subtitle 



Physiology of Prolonged Bed Rest 



5. Report Date 

August 1988 



6. Performing Organization Code 



7. Author(s) 

J. E. Greenleaf 



8. Performing Organization Report No. 

A-88214 



9. Performing Organization Name and Address 

Ames Research Center 
Moffett Field, CA 94035 



10. Work Unit No. 

199-21-12-07 



11. Contract or Grant No. 



12. Sponsoring Agency Name and Address 

National Aeronautics and Space Administration 
Washington, DC 205^6-0001 



13. Type of Report and Period Covered 

Technical Memorandum 



14. Sponsoring Agency Code 



15. Supplementary Notes 



Point of Contact; 



John Greenleaf, Ames Research Center, MS 239-17 

Moffett Field, CA 94035 (415) 694-6604 or FTS 464-6604 



16. Abstract 

Rest in bed has been a normal procedure used by physicians for centuries in the treatment of injury 
and disease. Exposure of patients to prolonged bed rest {>2H hr) in the horizontal position induces 
adaptive deconditioning responses. Thus "healing" proceeds concomitantly with deconditioning. While 
deconditioning responses are appropriate for patients or test subjects in the horizontal position, they 
usually result in adverse physiological responses, such as fainting and muscular weakness, when the 
patients assume the upright posture. These deconditioning responses result from reduction in hydro- 
static pressure within the cardiovascular system, virtual elimination of longitudinal pressure on the 
long bones, some decrease in total -body metabolism (exercise), changes in diet, and perhaps psychologi- 
cal impact from the different environment. Essentially every system in the body is affected by bed-rest 
deconditioning. An early stimulus is the cephalic shift of fluid from the legs which increases atrial 
pressure and induces compensatory responses for fluid and electrolyte redistribution. Without counter- 
measures, deterioration in strength and muscle function occurs within 1 wk while increased calcium loss 
may continue for months. In addition to problems with the cardiovascular, muscle and bone systems, 
increased research efforts should be focused on the effects of deconditioning on drug and carbohydrate 
metabolism, and the immune system. 



17. Key Words (Suggested by Aulhor(s)l 

Bed-rest deconditioning 
Remedial exercise training 
Fluid-electrolyte metabolism 
Hydrostatic pressure 
Carbohydrate metabolism 



19. Security Classif. (of this report) 

Unclassified 



18. Distribution Statement 

Unclassified-Unlimited 



Subject Category - 51 



20. Security Classif. (of this page) 

Unclassified 



21. No. of pages 

9 



22. Pricp 



NASA FORM 1626 OCT 86 



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