| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 The Spinal Cord Damage Research Center, 2 Departments of Medicine and Rehabilitation Medicine, Mount Sinai Medical Center, New York 10029; 3 Medical Service, Veterans Affairs Medical Center, Bronx 10468; and 4 Body Composition Unit, Columbia University-St. Luke's/Roosevelt Hospital Center, New York, New York 10025
 |
ABSTRACT |
|---|
 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
To determine the effect of paralysis on body composition,
eight pairs of male monozygotic twins, one twin in each pair with paraplegia, were studied by dual-energy X-ray absorptiometry. Significant loss of total body lean tissue mass was found in the paralyzed twins compared with their able-bodied co-twins: 47.5 ± 6.7 vs. 60.1 ± 7.8 (SD) kg (P < 0.005). Regionally, arm lean tissue mass was not different between the twin pairs, whereas trunk and
leg lean tissue masses were significantly lower in the paralyzed twins:
3.0 ± 3.3 kg (P < 0.05) and 10.1 ± 4.0 kg
(P < 0.0005), respectively. Bone mineral content of the total
body and legs was significantly related to lean tissue mass in the able-bodied twins (R = 0.88 and 0.98, respectively) but not in the paralyzed twins. However, the intrapair difference scores for bone
and lean tissue mass were significantly related (R = 0.80 and
0.81, respectively). The paralyzed twins had significantly more total
body fat mass and percent fat per unit body mass index than the
able-bodied twins: 4.8 kg (P < 0.05) and 7 ± 2% (P < 0.01). In the paralyzed twins, total body lean tissue was
significantly lost (mostly from the trunk and legs), independent of
age, at a rate of 3.9 ± 0.2 kg per 5-yr period of paralysis
(R = 0.87, P < 0.005). Extreme disuse from paralysis
appears to contribute to a parallel loss of bone with loss of lean
tissue in the legs. The continuous lean tissue loss may represent a
form of sarcopenia that is progressive and accelerated compared with
that in ambulatory individuals.
paraplegia; lean tissue mass; percent fat
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
AN INDIVIDUAL WITH SPINAL cord injury (SCI) and the resultant extreme disuse has a predisposition to medical consequences and secondary disabilities, such as lipid abnormalities (5, 8, 12), carbohydrate intolerance (5, 15), and cardiovascular disease (3, 4, 6). One hypothesis for these secondary disabilities of extreme disuse consists of the adverse changes in body composition (33, 38, 39), which may contribute to insulin resistance and associated disorders. Previous investigators, by using cross-sectional designs comparing age- and height-matched reference populations, have demonstrated lean tissue loss and/or fat tissue gain in individuals with SCI (13, 23, 24, 38). Because of wide individual variability in body composition and the absence of premorbid body composition measurements, a study employing a cross-sectional design is inherently limited in accurately determining the amount of lean tissue lost and fat tissue gained that is attributable exclusively to paralysis. Longitudinal studies are relatively expensive and pose enormous logistical problems, including performing measurements before the body composition changes have occurred, immediately after SCI, a time when the patient is often medically unstable or reluctant to participate in a research study. The task of recruiting subjects to perform these measurements intermittently over ensuing decades is problematic. Thus a creative solution to defining these changes in body composition that is independent of genetic variability and aging is a monozygotic twin model in which one twin has paralysis from traumatic SCI.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Subjects. Eight pairs of healthy identical twins, a paralyzed and an able-bodied twin, were studied. The subjects were recruited throughout the United States. To control for known variability within individuals with SCI, a group similar for gender and level and completeness of injury was selected to participate in the study. All subjects were men with motor complete paraplegia, levels T6-L1. None of the paralyzed twins was able to bear weight or had voluntary movement below the level of lesion since the time of injury. The duration of injury was 3-26 yr. All paralyzed twins used their arms daily for wheelchair mobility and were able to transfer independently. The able-bodied and paralyzed twins were in good health with no present known medical problems. The subjects were provided verbal and written information about the study, and written consent was obtained. Institutional Review Board approvals from the Veterans Affairs Medical Center and the Mount Sinai Medical Center were obtained for the study.
Genetic testing for zygosity was performed in all pairs at six independent, highly polymorphic loci (Lifecodes, Stamford, CT). All eight pairs were found to be strongly consistent with monozygosity, with a probability of being nonidentical of 1 in 4,096.Body composition studies. Height was measured in the standing position for the able-bodied twins and in the supine position with the subject fully extended for the paralyzed twins. Weight was measured on a Weight-Tronix scale (Scale Electronics Development, New York, NY). Body mass index (BMI) was calculated as total body wt (kg) / height (m2). The soft tissue compartments of fat and lean tissue mass were measured by dual-energy X-ray absorptiometry (DXA) on a total body scanner (model DPX, Lunar Radiation, Madison, WI) with the methods described by Wang et al. (40), Pierson et al. (31), Heymsfield et al. (26), and Mazess et al. (30). Calibration of DXA consisted of six graded mixtures of lean beef and fat, ranging from 3.7 to 85.6% fat, as measured by chemical analysis (31, 40). The subjects were asked to lie on a table, and whole body scanning was carried out with a congruent beam of stable dual-energy radiation (<1 mrem) at 40 and 70 keV; the radiation passed through the patient from below while the differential absorption was measured above. The ratio of absorption between the two X-rays of different energies was linearly related to the fat tissue mass in the soft tissue compartment. The procedure for scanning was ~30 min in duration and was well tolerated by all subjects studied. DXA provides a three-compartment partition of the body: bone mineral, fat mass, and fat-free mass. Lean tissue was calculated by the subtraction of bone mineral (g) from the fat-free mass (g). The precision and accuracy of DXA for soft tissue and bone have been reported to be ~99% with <1% error (29). Total body and regional percent fat were calculated as a percentage of soft tissue mass, with the skeleton and skull excluded. A previous detailed report has addressed the changes in the skeleton in these twins (7).
Statistical analyses.
Values are means ± SD. Unpaired t-tests were performed to
determine group differences, and paired t-tests were used to
determine significant differences within the pairs. Intrapair
difference (IPD) scores (paralyzed twin able-bodied twin) were
calculated within the twin pairs for body weight, total body and
regional bone mineral content (BMC), and lean and fat tissue
measurements. Linear regression analyses were used to plot lean and fat
tissue mass IPDs as a function of weight IPD. Effect size and power
calculations were performed on the variables.
| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
A relatively young group of twins was studied (40 ± 10, range
25-58 yr). The mean duration of injury for the twins with
paralysis was 16 ± 9 (range 3-26) yr. Height was similar for
both sets of twins. Weight and BMI were significantly lower in the
twins with paralysis than in their able-bodied co-twins: 71.4 vs. 81.5 kg (P < 0.05) and 22.3 vs. 25.4 kg/m2 (P < 0.05), respectively (Table 1).
|
Total body and regional lean tissue and BMC.
The twins with paralysis had significantly less total body, leg, and
trunk lean tissue than the able-bodied co-twins. Arm lean tissue mass
was not significantly different between the twin groups (Fig.
1). The mean total body lean tissue loss in
the twins with SCI was 12.6 ± 7.9 kg (Table
2). The majority of this lean tissue
atrophy was found in the trunk and leg regions, which were significantly reduced in the twins with paralysis: 3.0 ± 3.3 kg (P < 0.05) and 10.1 ± 4.0 kg (P < 0.0005), respectively (Table 2). The power for total body and leg lean
tissue differences between the twin groups was 0.91 and 0.99, respectively.
|
|
|
|
|
Total body and regional fat tissue. The percent fat in the legs was 17.5 ± 11.7% (P < 0.005) higher in the paralyzed than in the able-bodied twins (Fig. 1). Total body, arm, and trunk fat mass or percent fat was not significantly different between the twin pairs (Fig. 1).
A significant linear relationship was found between BMI and fat mass for both groups (R = 0.75, P < 0.05 for paralyzed twins and R = 0.82, P < 0.01 for able-bodied twins). No significant difference was noted between the slopes of these relationships. With control for BMI by multiple regression, fat mass and percentage were significantly increased by an average of 4.8 ± 1.8 kg (partial r = 0.59, P = 0.02) and 7.2 ± 2.4% (partial r = 0.60, P = 0.01) per unit of BMI in subjects with paralysis compared with the co-twins (Fig. 5).
|
10.1 ± 4.1 kg). The soft tissue compartments in
the leg changed in a direct linear relationship with total body weight
(Fig. 6). Thus, as the IPD for weight
increased, the IPD for lean and fat tissue also increased.
|
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Total body, leg, and trunk lean tissue mass were significantly reduced in the paralyzed twins. Although limited by sample size, the linear loss of total body and regional lean tissue mass with increasing duration of injury independent of age may be an important finding that has not previously been appreciated; this association would not have been observed without the use of a monozygotic twin controlled design.
Sarcopenia, or loss of muscle mass, occurs with aging (16, 27, 34). A variety of causes of sarcopenia have been postulated, one of which is disuse atrophy due to the decreased level of activity associated with aging (14). Young et al. (41) studied the cross-sectional area by ultrasound of the quadriceps muscle group in the able-bodied population in persons in their 20s and 80s. Comparison of the two groups showed a 25% decrease in the size of the quadriceps in the elderly group. In another study by Rice and co-workers (33) using computerized tomography, leg muscle size was reduced by 28-36% in subjects >65 yr of age. Our subjects with paralysis appear to exhibit an exaggerated form of sarcopenia, which is strongly associated with duration of injury and trends with age. The twins with paralysis at a mean age of 40 yr had already lost 20% of their total body mass and 48% of their leg lean tissue mass. This is twice the amount of leg muscle loss and 40 yr earlier than has been previously described in the general population (16, 27, 34).
Several studies have shown that physical activity delays loss of muscle mass with increasing age (9, 18, 19, 28). Our twins with SCI had an abrupt change in level of activity coincident with paralysis. Thus the identical-twin model has provided the design necessary to address whether adverse changes in lean tissue mass as a result of paralysis reach a new plateau or continue to show an age effect. Our findings suggest that chronic inactivity is associated with accelerated and progressive sarcopenia.
A strong correlation between change in body weight and change in total body lean mass has been well established (20, 21). Forbes et al. (22) reported a significant linear relationship between intrapair variation for lean body mass with intrapair variation for weight in monozygotic and dizygotic twins. In our study, total body weight was ~10 kg less in the paralyzed twins than in the able-bodied co-twins. The difference in weight was predominantly from loss of lean tissue in the leg. A direct association was found between intrapair body weight differences and loss of lean and fat tissues in the leg.
Total body percent fat was not significantly different between the twin pairs. Regional percent fat in the legs was significantly greater by an average of ~18% in paralyzed twins because of the combination of leg lean tissue loss and a slight increase in leg fat tissue. The able-bodied twins had an average of 1.3 kg less leg fat than the paralyzed twins. Bouchard et al. (10) reported in able-bodied persons that truncal-visceral fat increases with age, particularly in men. Neither total body fat nor regional fat mass was significantly related to age in the paralyzed or the able-bodied twin group, which was probably due to their relatively young ages.
In several studies of monozygotic twins reared apart, adult BMI and weights were reported to have heritability estimates of ~0.70 (1, 17, 30a, 39). In the general population, the relationship of fat mass with BMI is strong enough to use BMI as a surrogate measure for fat and as a screening for obesity (30a). In the twins with paralysis, a similar linear relationship for BMI with total body fat was noted, except this association was shifted to the left; the twins with SCI had ~5 kg more whole body fat mass and 7% more whole body fat than the able-bodied twins for any given unit of BMI. Further studies with a larger population base need to be performed to determine the validity of using BMI as a surrogate measure for obesity in those with SCI.
One could postulate that body composition variability between co-twins might account for some of the differences noted in our study. Several investigators have reported strong genetic components for lean tissue mass within monozygotic twin pairs (11, 22, 35). In a study by Forbes and colleagues (22) of 49 pairs of monozygotic and 38 pairs of same-gender dizygotic twins, lean body mass was found to have a 70% heritability estimate. Seeman et al. (35) reported that genetic factors account for 60-80% of the variance in lean mass (35). Bouchard et al. (10) studied 87 pairs of monozygotic and 66 pairs of dizygotic twins and reported a highly significant genetic component for body composition with heritability estimates of 50-80%. The differences observed within our twin pairs are far in excess of those that may be accounted for by differences attributable to normal or parallel environmental conditions within monozygotic twins.
In the paralyzed twins, level of injury was not found to have a significant correlation with the absolute lean tissue or the regional lean tissue loss. It should be appreciated that all subjects with SCI in this study were motor complete with lower paraplegia and had similar levels of function. We should expect to find an association between level of spinal lesion and total body lean tissue mass if subjects with higher and lower levels of injury with greater degrees of variation in neurological impairment were to be studied.
In the nonparalyzed population, it is widely accepted that a strong correlation exists between lean tissue mass and bone density (2, 35). Arden and Spector (2) used monozygotic and dizygotic twins to study the genetic components of muscle mass, muscle strength, and bone mineral density. They reported heritability estimates of 0.52 for lean body mass and 0.46 for leg strength. Lean body mass explained 6-16% of the variance of bone mineral density (2). In our study we found a strong correlation between total body and leg lean and bone tissues for the able-bodied twins but not for the paralyzed twins. This was probably due to the extreme loss in both parameters (lean and bone) in all twins with SCI. Although the absolute values for lean tissue and bone did not correlate in the twins with paralysis, the IPD scores for total body and leg lean tissue and BMC were well correlated, demonstrating a close relationship between bone and lean tissue loss.
In conclusion, in persons with paralysis from SCI, there is an accelerated form of sarcopenia, similar to that seen in the elderly during the sixth through the eighth decades of life. SCI appears to cause a chronic catabolic state, whereby total body lean tissue, albeit mostly from the legs in our subjects with lower SCI, is depleted at a rate of ~8 kg/decade, about twice the rate of matched controls. Loss of lean tissue is linearly related to loss of BMC. Without the use of an identical- twin model discordant for paralysis, the progression and severity of lean tissue loss throughout the chronic phase of immobilization could not have been identified with this degree of accuracy. In individuals with chronic immobilizing conditions, further studies with identical twins may identify other potential body composition changes, as well as hormonal and metabolic alterations, that may be associated with these body composition changes.
| |
ACKNOWLEDGEMENTS |
|---|
This research was supported by grants from the Spinal Cord Research Foundation (Washington, DC), the Eastern Paralyzed Veterans Association (Jackson Heights, NY), the Veterans Affairs Medical Center (Bronx, NY), and The Mount Sinai Medical Center (New York, NY).
| |
FOOTNOTES |
|---|
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: A. M. Spungen, Spinal Cord Damage Research Center, Veterans Affairs Medical Center, Rm. 1E-02, 130 West Kingsbridge Rd., Bronx, NY 10468 (E-mail: AmSpungen{at}worldnet.att.net).
Received 15 October 1998; accepted in final form 23 November 1999.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Allison, DB,
Kaprio J,
Korkeila M,
Neale MC,
and
Hayakawa K.
The heritability of body mass index among an international sample of monozygotic twins reared apart.
Int J Obes
20:
501-506,
1996[ISI][Medline].
2.
Arden, NK,
and
Spector TD.
Genetic influences on muscle strength, lean body mass, and bone mineral density: a twin study.
J Bone Miner Res
12:
2076-2081,
1997[ISI][Medline].
3.
Bauman, WA,
Raza M,
and
Machac J.
Tomograhic thallium-201 myocardial perfusion imaging after intravenous dipyridamole in asymptomatic subjects with quadriplegia.
Arch Phys Med Rehabil
I74:
740-744,
1993[ISI][Medline].
4.
Bauman, WA,
Raza M,
Spungen AM,
and
Machac J.
Upper ergometry cardiac stress testing with thallium-201 imaging in paraplegia.
Arch Phys Med Rehabil
75:
946-950,
1994[ISI][Medline].
5.
Bauman, WA,
and
Spungen AM.
Disorders of carbohydrate and lipid metabolism in veterans with paraplegia or quadriplegia: a model of premature aging.
Metabolism
43:
949-956,
1994.
6.
Bauman, WA,
Spungen AM,
Rothstein J,
Tsuruta M,
Zhang RL,
Zhong YG,
Shahidi R,
Raza M,
Pierson RN, Jr,
Wang J,
and
Gordon SK.
Coronary artery disease: metabolic risk factors and latent disease in individuals with paraplegia.
Mt Sinai J Med
59:
163-168,
1992[Medline].
7.
Bauman, WA,
Spungen AM,
Wang J,
Pierson RN, Jr,
and
Schwartz E.
Continuous loss of bone in chronic immobilization: a monozygotic twin study.
Osteoporosis Int
10:
123-127,
1999[ISI][Medline].
8.
Bauman, WA,
Spungen AM,
Zhong YG,
Zhang RL,
Petry C,
and
Gordon SK.
Depressed serum high density lipoprotein cholesterol levels in veterans with spinal cord injury.
Paraplegia
30:
697-703,
1992[ISI][Medline].
9.
Booth, FW,
Weeden SH,
and
Tseng BS.
Effect of aging on human skeletal muscle and motor function.
Med Sci Sports Exerc
26:
556-560,
1994[ISI][Medline].
10.
Bouchard, C,
Despres J-P,
and
Mauriege P.
Genetic and nongenetic determinants of regional fat distribution.
Endocr Rev
14:
72-93,
1993[Abstract].
11.
Bouchard, C,
Savard R,
Depres J-P,
Tremblay A,
and
Leblanc C.
Body composition in adopted and biological siblings.
Hum Biol
57:
61-75,
1985[ISI][Medline].
12.
Brenes, G,
Dearwater S,
Shapera R,
LaPorte RE,
and
Collins E.
High density lipoprotein cholesterol concentrations in physically active and sedentary spinal cord injured patients.
Arch Phys Med Rehabil
67:
445-450,
1986[ISI][Medline].
13.
Cardus, D,
and
McTaggart WG.
Body composition in spinal cord injury.
Arch Phys Med Rehabil
66:
257-259,
1985[ISI][Medline].
14.
Carmeli, E,
and
Reznick AZ.
The physiology and biochemistry of skeletal muscle atrophy as a function of age.
Proc Soc Exp Biol Med
206:
103-113,
1994[Abstract].
15.
Duckworth, WC,
Solomon SS,
Jallepalli P,
Heckemeyert C,
Finnern J,
and
Powers A.
Glucose intolerance due to insulin resistance in patients with spinal cord injuries.
Diabetes
29:
906-910,
1980[Abstract].
16.
Evans, WJ,
and
Campbell WW.
Sarcopenia and age-related changes in body composition and functional capacity.
J Nutr
123:
465-468,
1993.
17.
Fabsitz, RR,
Sholinsky P,
and
Carmelli D.
Genetic influences on adult weight gain and maximum body mass index in male twins.
Am J Epidemiol
140:
711-720,
1994
18.
Fielding, RA.
The role of progressive resistance training and nutrition in the preservation of lean body mass in the elderly.
J Am Coll Nutr
14:
587-594,
1995[Abstract].
19.
Fielding, RA.
Effects of exercise training in the elderly: impact of progressive-resistive training on skeletal muscle and whole-body protein metabolism.
Proc Nutr Soc
54:
665-675,
1996.
20.
Forbes, GB.
Lean body mass-body fat interrelationships in humans: dietary changes induce changes in both body components.
Nutr Rev
45:
225-231,
1987[ISI][Medline].
21.
Forbes, GB.
Human Body Composition: In Vivo Methods, Models and Assessment. New York: Plenum, 1993, p. 1-14.
22.
Forbes, GB,
Sauer EP,
and
Weitkamp LR.
Lean body mass in twins.
Metabolism
44:
1442-1446,
1995[ISI][Medline].
23.
George, CM,
Wells CL,
and
Dugan NL.
Validity of hydrodensitometry for determination of body composition in spinal cord injured subjects.
Hum Biol
60:
771-780,
1988[ISI][Medline].
24.
Greenway, RM,
Houser HB,
Lindan O,
and
Weir DR.
Long-term changes in gross body composition of paraplegic and quadriplegic patients.
Paraplegia
7:
301-318,
1970[Medline].
26.
Heymsfield, SB,
Wang J,
Heshka S,
Kehayias JJ,
and
Pierson RN, Jr.
Dual-photon absorptiometry: comparison of bone mineral and soft tissue mass measurements in vivo with established methods.
Am J Clin Nutr
49:
1283-1289,
1989
27.
Holloszy, JO.
Workshop on sarcopenia: muscle atrophy in old age.
J Gerontol
50A:
1-161,
1995.
28.
Horber, FF,
Kohler SA,
Lippuner K,
and
Jaeger P.
Effect of regular physical training on age-associated alteration of body composition in men.
Eur J Clin Invest
26:
279-285,
1996[ISI][Medline].
29.
Lukaski, HC.
Soft tissue composition and bone mineral status: evaluation by dual-energy X-ray absorptiometry.
J Nutr
123:
438-443,
1993.
30.
Mazess, RB,
Peppler WW,
and
Gibbons M.
Total body composition by dual-photon absorptiometry.
Am J Nutr
40:
834-839,
1984
30a.
National Institutes of Health Consensus Development Panel on the Health Implications of Obesity.
Health implications of obesity.
In: National Institutes of Health Consensus Development Conference Statement Annals of Internal Medicine. Bethesda, MD: National Institutes of Health, 1985, vol. 103, p. 1073-1077.
31.
Pierson, RN, Jr,
Wang J,
Heymsfield SB,
Russell-Aulet M,
Mazariegos M,
Tierney M,
Smith R,
Thornton JC,
Kehayias J,
Weber DA,
and
Dilmanian FA.
Measuring body fat: calibrating the rulers. Intermethod comparisons in 389 normal Caucasian subjects.
Am J Physiol Endocrinol Metab
261:
E103-E108,
1991
32.
Rasmann Nuhlicek, DN,
Spurr GB,
Barboriak JJ,
Rooney CB,
El Ghatt AZ,
and
Bongard RD.
Body composition of patients with spinal cord injury.
Eur J Clin Nutr
42:
765-773,
1988[ISI][Medline].
33.
Rice, CL,
Cunningham DA,
and
Paterson DH.
Arm and leg composition determined by computer tomography in young and elderly men.
Clin Physiol
9:
207-220,
1985.
34.
Roubenoff, R,
Heymsfield SB,
Kehayias JL,
Cannon JG,
and
Rosenberg IH.
Standardization of nomenclature of body composition in weight loss.
Am J Clin Nutr
66:
192-196,
1997
35.
Seeman, E,
Hopper JL,
Young NR,
Formica C,
Goss P,
and
Tsalamandris C.
Do genetic factors explain associations between muscle strength, lean mass, and bone density: a twin study.
Am J Physiol Endocrinol Metab
270:
E320-E327,
1996
36.
Shizgal, HM,
Roza A,
Leduc B,
Drouin G,
Villemure J-G,
and
Yaffe C.
Body composition in quadriplegic patients.
J Parent Enteral Nutr
10:
364-368,
1986[Abstract].
37.
Spungen, AM,
Bauman WA,
Wang J,
and
Pierson RN, Jr.
Measurement of percent body fat in individuals with quadriplegia: a comparison of eight clinical methods.
Paraplegia
33:
402-408,
1995[ISI][Medline].
38.
Spungen, AM,
Bauman WA,
Wang J,
and
Pierson RN, Jr.
The relationship between total body potassium and resting energy expenditure in individuals with paraplegia.
Arch Phys Med Rehabil
73:
965-968,
1993.
39.
Stunkard, AJ,
Harris JB,
Pedersen NL,
and
McClearn GE.
The body mass index of twins who have been reared apart.
N Engl J Med
322:
1483-1487,
1990[Abstract].
40.
Wang, J,
Heymsfield SB,
Aulet M,
Thornton JC,
and
Pierson RN, Jr.
Body fat from body density: underwater weighing vs. dual-photon absorptiometry.
Am J Physiol Endocrinol Metab
256:
E829-E834,
1989
41.
Young, A,
Stokes M,
and
Crowe M.
The size and strength of the quadriceps muscles in old and young men.
Clin Physiol
5:
145-154,
1985[ISI][Medline].
This article has been cited by other articles:
|
|
 |
|
  S. D. Primeaux, M. Tong, and G. M. Holmes Effects of chronic spinal cord injury on body weight and body composition in rats fed a standard chow diet Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2007; 293(3): R1102 - R1109. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. A. Bauman, A. M. Spungen, J. Wang, R. N. Pierson Jr., and E. Schwartz Relationship of fat mass and serum estradiol with lower extremity bone in persons with chronic spinal cord injury Am J Physiol Endocrinol Metab, June 1, 2006; 290(6): E1098 - E1103. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. A. Bauman, S. C. Kirshblum, N. G. Morrison, C. M. Cirnigliaro, R.-L. Zhang, and A. M. Spungen Effect of Low-Dose Baclofen Administration on Plasma Insulin-like Growth Factor-I in Persons With Spinal Cord Injury. J. Clin. Pharmacol., April 1, 2006; 46(4): 476 - 482. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. M. Modlesky, C. S. Bickel, J. M. Slade, R. A. Meyer, K. J. Cureton, and G. A. Dudley Assessment of skeletal muscle mass in men with spinal cord injury using dual-energy X-ray absorptiometry and magnetic resonance imaging J Appl Physiol, February 1, 2004; 96(2): 561 - 565. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Spungen, R. H. Adkins, C. A. Stewart, J. Wang, R. N. Pierson Jr., R. L. Waters, and W. A. Bauman Factors influencing body composition in persons with spinal cord injury: a cross-sectional study J Appl Physiol, December 1, 2003; 95(6): 2398 - 2407. [Abstract] [Full Text]
|
|
|
|
 |
|
 J. M. Wecht, R. E. De Meersman, J. P. Weir, A. M. Spungen, and W. A. Bauman Cardiac homeostasis is independent of calf venous compliance in subjects with paraplegia Am J Physiol Heart Circ Physiol, June 1, 2003; 284(6): H2393 - H2399. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. E. Morley, H. M. Perry III, and D. K. Miller Editorial: Something About Frailty J. Gerontol. A Biol. Sci. Med. Sci., November 1, 2002; 57(11): M698 - 704. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
P < 0.0005; 
P < 0.05.
)
and able-bodied (
) twins. In leg and total body, able-bodied twins
had highly significant relationships between BMC and lean tissue mass
(R = 0.88, P < 0.005 and R = 0.98, P < 0.0001, respectively), but no such relationship was found in
paralyzed twins.
