ORIGINAL CONTRIBUTION
Relationship of Spasticity to Soft Tissue Body Composition
and the Metabolic Profile in Persons With Chronic Motor
Complete Spinal Cord Injury#1

Ashraf S. Gorgey, PT, PhD1,2; Anthony E. Chiodo, MD2; Eric D. Zemper, PhD2; Joseph E. Hornyak, MD2;
Gianna M. Rodriguez, MD2; David R. Gater, MD, PhD1,3
1Spinal Cord Injury and Disorders Service, Hunter Holmes McGuire VA Medical Center, Richmond, Virginia;
Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, Michigan; 3Department of
Physical Medicine and Rehabilitation, Virginia Commonwealth University, Richmond, Virginia

2

Received January 14, 2009; accepted June 29, 2009
Abstract
Background/Objective: To determine the effects of spasticity on anthropometrics, body composition(fat mass [FM] and fat-free mass [FFM]), and metabolic profile (energy expenditure, plasma glucose, insulin
concentration, and lipid panel) in individuals with motor complete spinal cord injury (SCI).
Methods: Ten individuals with chronic motor complete SCI (age, 33 ± 7 years; BMI, 24 ± 4 kg/m2; level of
injury, C6–T11; American Spinal Injury Association A and B) underwent waist and abdominal
circumferences to measure trunk adiposity. After the first visit, the participants were admitted to thegeneral clinical research center for body composition (FFM and FM) assessment using dual energy x-ray
absorptiometry. After overnight fasting, resting metabolic rate (RMR) and metabolic profile (plasma
glucose, insulin, and lipid profile) were measured. Spasticity of the hip, knee, and ankle flexors andextensors was measured at 6 time points over 24 hours using the Modified Ashworth Scale.
Results: Knee extensor spasticity was negatively correlated to abdominal circumferences (r 5 20.66, P 5
0.038). After accounting for leg or total FFM, spasticity was negatively related to abdominal circumference(r 5 20.67, P 5 0.03). Knee extensor spasticity was associated with greater total %FFM (r 5 0.64; P 5
0.048), lower %FM (r 5 20.66; P 5 0.03), and lower FM to FFM ratio. Increased FFM (kg) was associatedwith higher RMR (r 5 0.89; P 5 0.0001). Finally, spasticity may indirectly influence glucose homeostasis andlipid profile by maintaining FFM (r 5 20.5 to 20.8, P , 0.001).
Conclusion: Significant relationships were noted between spasticity and variables of body composition andmetabolic profile in persons with chronic motor complete SCI, suggesting that spasticity may play a role in the
defense against deterioration in these variables years after injury. The exact mechanism is yet to be determined.
J Spinal Cord Med. February 2010;33(1):6–15
Key Words: Spasticity; Body composition; Resting energy expenditure; Metabolism; Spinal cord injuries;
Paraplegia; Tetraplegia; Cardiovascular disease
INTRODUCTION
Please address correspondence to Ashraf Gorgey, PT, PhD,
Spinal Cord Disorders Service, Hunter Holmes McGuire VA
Medical Center, 1201 Broad Rock Boulevard, Richmond, VA
23249; p: 804 675 5000, ext 3603; f: 804 675 5223 (e-mail:ashraf.gorgey@va.gov; agorgey@gmail.com).
This work was supported through funding of Scholarship to
Advance Research in Spasticity (STARS) Foundation, National
Institute on Disability and Rehabilitation Research (NIDRR)
Grant H133P030004, and the General Clinical Research Center(NIH Funding to the University of Michigan).
G 2010 by the American Paraplegia Society

6

Spinal cord injury (SCI) results in complete or incomplete
insult to the spinal cord with extensive skeletal muscle
paralysis below the level of injury (1,2). The reduced
neuromuscular activity after SCI coupled with a reductionin physical activity is accompanied by a dramatic deterioration in body composition and metabolic profile (3–8).
In the first few months after injury, there is a rapid onset ofskeletal muscle atrophy, increase of fat mass (FM), anddecrease of fat-free mass (FFM) (4,7). For example, skeletal
muscle cross-sectional area could be as low as 30% to 50%
compared with able-bodied (AB) controls (9,10). Moreover, evidence has shown that %FM could easily exceed
30% in individuals with chronic SCI (8,11).

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The loss of metabolically active lean tissue results in
reduction of the basal energy expenditure in people
with SCI (3,12,13). Energy expenditure and basal
metabolic rate are lower even after adjusting for their
FFM compared with healthy AB controls (12,13),predisposing them to a great risk of developing obesity(14,15). Individuals with SCI have more FM and lower
energy expenditure compared with their monozygotic
siblings without SCI (12). The changes in bodycomposition after SCI are associated with numerous
metabolic abnormalities, including glucose intolerance,
insulin resistance (4–6), hyperlipidemia (5,6), andcardiovascular diseases (16). Recently, it was reported
that 55% of individuals with SCI are at risk ofdeveloping metabolic syndrome (17). This could resultin a shortened life span and health-related complications of socioeconomic burdens that negatively decrease the perceived quality of life after SCI and may
interfere with their degree of independence andintegration into the community (18).
The factors that influence the deterioration inenergy expenditure, body composition, and metabolic
profile after SCI are poorly understood. Understanding
these factors may help to enhance the quality of life after
SCI by providing appropriate medical and rehabilitationinterventions. Spasticity is an upper motor neuron
disorder that affects 70% of patients with chronic
cervical and thoracic level injuries 1 year after injury(19). Spasticity is a complex phenomenon of exaggerated muscle tone, reflexes, and clonus that affects theskeletal muscles below the level of injury (19,20).
Spasticity has often been viewed as a factor that cannegatively impact functional progress after SCI (19,20).
Despite its negative influence, spasticity could beviewed as expressing positive features (21,22). For
example, spasticity has been shown to improve ambulation and peripheral circulation (23,24). Moreover,spasticity in the tail muscle of rats has proven topreserve the slow properties of skeletal muscle andattenuate the slow-to-fast transformation in myosin
expression and myofiber atrophy that commonly occurs
after SCI (25,26). Most recently, spasticity has beenshown to defend against the process of skeletal muscle
atrophy as early as 6 weeks after injury (21) and improveglucose homeostasis (22). Spastic thigh skeletal muscle
size was 22% larger compared with the flaccid group(21). Moreover, glucose uptake was 3 times higher inthe spastic limbs compared with controls (22).
Therefore, the purpose of this study was to investigate the protective effects of spasticity on whole bodycomposition (FM and FFM) and metabolic profile(glucose tolerance, insulin sensitivity, and lipid profile)in chronic SCI. Additionally, the relationship between
spasticity and resting metabolic rate (RMR) was studied.
It is hypothesized that spasticity could positively attenuate the deterioration in body composition and metabolic profile in individuals with chronic SCI.

METHODS
Ten individuals with chronic traumatic motor complete
SCI (8 men and 2 women; mean ± SD: age, 33 ± 7
years; body weight, 72 ± 11 kg; height, 176 ± 11 cm;
level of injury, C6–T11; American Spinal Injury Association [ASIA] classification A, B) participated in the study.
All participants were recruited from the university model
SCI system and from Spasticity Clinic. Detailed descriptions for all procedures and risks of participation in thisstudy were provided to each potential participant. All
subjects gave written informed consent before the study.
The institutional review board of The University ofMichigan approved this study.
Participants were included if they were (a) men or
women 18 to 45 years of age, with the maximum age
chosen to avoid any confounding effects of the aging
process on body composition and energy expenditures;(b) a minimum of 1 year after injury and had been
maintained for 1 year on the same dose of oral baclofen,
an antispasticity medication, to ensure stability of
spasticity at the time of measurements; (c) the level of
injury was C6 to T11. People with injury above C6 have
limited hand functions and are dependent on others to
prepare their meals or they potentially eat less. This could
potentially result in lower body mass compared withother groups and influence their whole body composition. Lower motor neuron injury is typically found in
those with injury below T11 and leads to flaccid paralysisof the involved skeletal muscles that ultimately affects
body composition (21).
Participants were excluded from the study if they
had hypertension, diabetes mellitus or elevated serum
lipids, smoked or abused alcohol, had pressure ulcers
greater than grade II, or were taking medications that
affect metabolic profile, such as insulin. Individuals withbody mass index (BMI) greater than 30 kg/m2 were
excluded to avoid any confounding effects fromincreasing relative or absolute FM on the results.
Additionally, BMI underestimates the percentage ofFM in people with SCI (27). Etiologies for SCI other thantrauma and other clinical populations with spasticity
were excluded.
First Visit/Baseline Assessment
After undergoing a phone interview to determine
eligibility, the 10 participants who met the study
inclusion criteria were invited to the Health and Human
Performance Laboratory located at the Department of
Physical Medicine and Rehabilitation. The visit was timed
at 7 to 10 days before admission to the General ClinicalResearch Center (GCRC) at the University of Michigan.
On arrival, participants were asked to void their bladderand to undergo a general physical examination by acertified physician. The physical examination included
measuring vital signs and a resting 12-lead electrocardiogram performed to rule out any pre-existing cardiac
problems.

Spasticity, Body Composition, and Metabolic Profile7

Figure 1. A frame of the timeline of the study during the first visit at the laboratory and the second visit at the GCRC. Timepoints are numbered MAS (1) to MAS (6).
During the same visit, body weight (kg) and height(m) were measured to calculate their BMI (kg/m2). The
weight of the participant was measured on a wheelchairscale (Tanita, Arlington Heights, IL, USA). After theparticipant moved to the testing table, the wheelchair
was weighed empty and subtracted from the total
weight. Height was measured in a supine position fromthe top of the head to the heel.
Because of a technical difficulty, a subset of ourparticipants (n 5 5) underwent a graded exercise test on
an arm-crank ergometer (Monark Rehab Trainer 881E,
Stockholm, Sweden) to measure their maximum aerobic
capacity using a ParvoMedics (Sandy, UT) metabolic cart
at a constant room temperature of 22uC. After calibration
and assigning a nose clip, a sterilized mouth piece wassecured with head mounting. The protocol consisted of
2-minute stages of exercise with 30-second intervals ofrest to measure blood pressure. After 2 minutes of rest,
the participant started pedaling at a resistance of 25 W
and was asked to maintain a rate of 50 revolutions/min(RPM). Resistance was gradually increased by 25 W at theend of each 30-second rest interval. VO2 peak wasconsidered when respiratory exchange ratio values weregreater than 1.1 and they failed to maintain the assigned
cranking rate.
Anthropometrics
Waist (WC) and abdominal circumferences were measured using an inelastic tape measure at the level of thenarrowest part of the torso and at the umbilicus,
respectively (14). The measurements were taken insitting and supine positions, at the end of expiration,
and without compressing the skin. Careful attention wasmade to positioning the tape measure at the sameanatomical location when in sitting and supine positions.
Second Visit
The participants underwent a second visit to measure theirbody composition and metabolic profile. The timeline of theovernight 24-hour stay is presented in Figure 1. Participants
reported to the GCRC at the University of Michigan hospital.
After a routine physical examination, they underwent a bodycomposition assessment using lunar dual energy x-ray
absorptiometry (DEXA). After an overnight 12-hour fast,

8

RMR was measured after lying for 30 minutes in a darkroom. Data acquisition of the RMR was 20 minutes.
Modified Ashworth Scale
The Modified Ashworth scale (MAS) was used to evaluate
spasticity for hip, knee, and ankle skeletal muscle flexors
and extensors for both lower extremities (20,21,23).
Spasticity was evaluated in a supine position by the sameinvestigator (Table 1). The room temperature was held
constant at 21uC to 24uC. Spasticity was measured over
24 hours during an overnight stay at 2:00 PM, 5:00 PM,
and 8:00 PM (first day) and 5:00 AM, 7:00 AM, and 9:00 AM(second day) (Figure 2). This approach was considered toaccount for fluctuations in spasticity previously reported(23). The average score of the 3 time points (2:00 PM,
5:00 PM, and 8:00 PM) was considered for statisticalanalysis because this represents the magnitude of
spasticity on a daily basis under the effects of oral
baclofen. The 3 time points that were measured in themorning overestimated the magnitude of spasticity,
because participants were immobilized and delayed
administration of their dosage of oral baclofen until
concluding the metabolic study because oral baclofen is
known to influence the metabolic profile in people withSCI (28). Spasticity was adjusted to the leg-FFM because
spasticity was shown to explain portion of the variance inleg muscle size after SCI (21). The following equations
were used to clarify how a single score was assigned to anindividual muscle group (20).
MAS side (right or left individual muscle group) ~ð1Þ

the average of 3 trials:
MASt ~ (MASright z MASleft )=2,

ð2Þwhere t 5 1400, 1700, or 2000h.
A single score ~(MAS2 : 00 z MAS5 : 00 z MAS8 : 00)=3,

ð3Þ

Lower extremity (extensor or flexor) spasticity ~The Journal of Spinal Cord Medicine

MAShip z MASknee z MASankle:

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ð4Þ

Table 1. Six Grades of the MAS
Grade
0
1
2

3
4
5

Definition
No increase in skeletal muscle tone
Slight increase in skeletal muscle tone manifested by acatch and release at the end of the ROM
Slight increase in skeletal muscle tone, manifested by acatch, followed by minimal resistance throughout theROM
Considerable increase in skeletal muscle tone
More marked increase in skeletal muscle tone
throughout the ROM
Rigid in flexion or extension

ROM, range of motion.

Dual Energy X-Ray Absorptiometry
Body composition was measured using total body scanswith a Lunar Prodigy Advance scanner (Lunar DPX, DEXA
Scanner; Lunar, Madison, WI) (8,11). Regional (arms,
legs, trunk, gynoid, android) and total body %FM and%FFM were measured (Figure 3). An index of FM to FFM
was used to compare regional compartments. The
coefficient of variability of repeated scans was less than
3%.

Metabolic Profile
After an overnight fasting, participants underwent anarray of examinations to measure their metabolic profile.
At 6:00 AM, basal metabolic rate and respiratoryexchange ratio was measured by an indirect calorimetry
unit (Vmax metabolic cart; SensorMedics Vmax, Yorba
Linda, CA, USA) in a dark room located at the GCRC.
Participants were asked to lie in a dark room for 20 to
30 minutes to attain a resting state, after which RMR was
measured using a canopy-ventilated system for 20 minutes. The gases (VCO2 and VO2) were collected to measure
the respiratory exchange ratio and to calculate resting
whole body rate of fat oxidation using the equation of
Fryan (29).
Afterward, a Teflon catheter was inserted into anantecubital vein of 1 arm for blood sampling, and 4 mL/
subject was sent for the analysis of triglycerides (TG),
total cholesterol, high-density lipoprotein (HDL), andlow-density lipoprotein (LDL). After allowing the blood
sample to clot for 30 minutes, the blood was centrifuged
at 3,000 RPM for 10 minutes, and the serum wastransferred for analysis.
At 7:00 AM, a standard 75-g oral glucose tolerance test
(OGTT) was administered, and blood was drawn at
0 minute before and 30, 60, 90, and 120 minutes afteradministration. A 4-mL sample of blood was drawn at eachtime point to measure plasma glucose and insulin

Figure 2. The average of spasticity scores of (a) hip, (b) knee, and (c) ankle flexors and extensors over the course of
24 hours. Hypertonicity was more in the extensor skeletal muscle groups compared with the flexors. A pattern of increased
hypertonicity was detected in the morning because of immobilization and late administration of their oral baclofen dose.

Spasticity, Body Composition, and Metabolic Profile

9

Figure 3. Mean ± SD of %FM and %FFM using lunar DEXA for the measurement of regional and total body composition.
concentrations. All blood samples were sent to theChemistry Pathology Laboratory for analysis. The plasma
concentrations of TGs and glucose concentrations were
determined using commercially available colorimetricassays (Sigma, Wako, St. Louis, MO, USA and Thermo
DMA, Arlington, TX, USA, respectively). The plasma insulin
concentration was measured using a commercially available radioimmunoassay kit (Linco Research, St. Charles,
MO, USA). Insulin sensitivity was determined using the
Matsuda and Defronzo formula: Insulin sensitivity 5
10.000/sq. root (Fasting plasma glucose 3 fasting plasma
insulin) 3 (mean OGTT glucose concentration 3 mean
OGTT insulin concentration) (30). Additionally, the HOMA
index was calculated as the product of the fasting plasma
insulin level (mU/mL) and the fasting plasma glucose level(mmol/L), divided by 22.5. Finally, the areas under the
curve (AUC) for plasma glucose and insulin were computed by integration with trapezoidal rule.
Statistical Analysis
Considering the ordinal nature of MAS, Spearman r
correlation was used to determine the relationshipbetween spasticity, body composition, RMR, and metabolic profile. The Pearson correlation was used todetermine the relationship among body composition,
RMR, and metabolic profile variables. A continuous design
was used because the current population is characterizedby many confounding factors, and matching between 2
groups is extremely difficult. Partial correlations were used
to adjust for time since injury and oral baclofen dose for all
the studied variables. Repeated-measure analysis of variance was used to test for differences among the indices of
FM to FFM of arms, legs, trunk, and total body. All values
are presented as mean ± SD, and statistical significancewas set at a level of P , 0.05.
RESULTS
The time since injury was 11 ± 7 years (range, 2–22
years). BMI of the subjects was 24 ± 4 kg/m2. VO2 peak10

was 0.92 ± 0.3 L/min (13.05 ± 4.5 mL/kg/min),suggesting low exercise tolerance.
Spasticity
The outcomes of MAS of the 6 skeletal muscle groups
over 24 hours are presented in Figure 2. The sum of hip,knee, ankle flexor and extensor spasticity was 4.5 ± 2
and 6 ± 3, respectively (P 5 0.001). Spasticity scores of
the hip flexors vs extensors were 2.1 ± 0.9 vs 2.4 ± 0.9(P 5 0.08), knee flexors vs exstensors were 2.0 ± 0.8 vs
2.6 ± 1.0 (P 5 0.005), and ankle flexors vs exstensors
were 2.0 ± 0.8 vs 2.5 ± 1.0 (P 5 0.055).
Spasticity and Anthropometrics
The average of the lower extremity flexor or extensor
spasticity was not related to WCs and abdominal
circumferences. However, there were trends toward anegative association between knee flexor (r 5 20.60, P
5 0.064) or extensor spasticity (r 5 20.57, P 5 0.08)
and abdominal circumference in the lying position. The
average of extensor spasticity (hip, knee, and ankle)
adjusted to total body FFM or leg FFM was negatively
related to abdominal circumferences (r 5 20.67, P 50.03). Knee extensor spasticity was negatively correlated
to abdominal circumferences (r 5 20.66, P 5 0.038).
There were trends toward negative associations with WC(r 5 20.56 and 20.6), but they did not attainsignificance (P . 0.5).
Spasticity and Body Composition
Total body composition assessment showed that %FFM
and %FM were 64 ± 6% and 36 ± 6%, respectively(Figure 3). Increasing knee extensor spasticity was associated with a reduction in the %FM of the gynoid region (r 520.65, P 5 0.047; Figure 4a), trunk (r 5 20.65, P 5
0.039), and total body (r 5 20.65, P 5 0.03; Figure 4b),but not leg %FM. Additionally, increasing knee flexor
spasticity was associated with reduction in trunk and total%FM (r 5 20.73, P 5 0.016 and r 5 20.64, P 5 0.048,
respectively). Knee extensor spasticity was directly associ-

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Figure 4. Inverse relationships between knee extensors spasticity and %FM in (a) gynoid (r 5 20.65, P 5 0.047) and (b)total body (r 5 20.65, P 5 0.03) and indices of FM to FFM in (c) trunk (r 5 20.69, P 5 0.025) and (d) total body (r 520.65, P 5 0.04).
ated with an increase in %FFM in the gynoid region andtotal body (r 5 0.63 and 0.65, respectively, P , 0.03).
Additionally, knee flexor spasticity was directly associatedwith an increase in % FFM in the trunk (r 5 0.73, P 5 0.01)
and total body (r 5 0.64, P 5 0.048).
The ratio of FM/FFM was 0.73 ± 0.23, 0.36 ± 0.20,
0.57 ± 0.13, and 0.56 ± 0.15 in leg, arm, trunk, andtotal body composition, respectively (P 5 0.0001).
Pairwise comparisons showed significant differences
between the ratio in legs and arms (P 5 0.0001) andarms and trunk (P 5 0.038), suggesting an increase in
the fat mass in legs and trunk compared with the arms.
The average of knee extensor spasticity was negatively
related to the ratio of FM/FFM of legs (r 5 20.56, P 50.08), trunk (r 5 20.69, P 5 0.025), and total body (r 520.65, P 5 0.04; Figure 4c and d).
Spasticity and Metabolic Profile
The RMR was 1,256 ± 231 kcal/d. The respiratoryexchange ratio was 0.76 ± 0.05 and fat oxidation was
71 ± 20 g/min. Increased FFM (kg) was associated withhigher RMR (r 5 0.89; P 5 0.0001; Figure 5); however,spasticity did not influence RMR. Knee extensor and flexor
spasticity adjusted to leg FFM showed a strong association
with fat oxidation (r 5 0.46 and 0.57; P 5 0.08).

Fasting plasma glucose and insulin were 87 ±10 mg/dL and 13 ± 3 mm/mL, respectively. Afteradministering the OGTT, plasma glucose increased to
132 ± 28, 121 ± 30, 113 ± 27, and 117 ± 31 mg/dL at
30, 60, 90, and 120 minutes, respectively. Plasma insulin
increased to 106 ± 51, 100 ± 49, 72 ± 41, and 74 ±49 mm/mL at the corresponding time points. The Homeostatic Model of Assessment index was 2.8 ± 0.8, andinsulin sensitivity using the Mostuda and Defronzo
formula was 3.8 ± 1.8. The AUCs for glucose and insulin

Figure 5. The relationship between FFM-total body (kg)and RMR (kcal/d; r 5 0.89; P 5 0.0001).

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11

Table 2. Outcomes of the Lipid Profile After Overnight Fasting at the GCRC (n 5 10)

Plasma concentration%FFM-lega%FFM-trunka%FFM-totala

Cholesterol (mg/dL)

HDL (mg/dL)

Triglycerides (mg/dL)

LDL (mg/dL)

176 ± 38
20.89 (0.001)
20.69 (0.03)
20.91 (0.001)

44.4 ± 5.9
NS
NS
NS

115 ± 50
20.67 (0.049)
20.46 (0.21)
20.69 (0.38)

139 ± 40
20.87 (0.003)
20.69 (0.038)
20.88 (0.002)

aPartial correlation, (P values) after adjusting for oral baclofen dose.
NS, nonsignificant correlation.

were 672 ± 127 and 408 ± 171, respectively. A trend of
reduction in plasma glucose at T120 was associated withan increase in %FFM-total (r 5 20.59, P 5 0.06). %FFM
leg was associated with a reduction in glucose AUC (r 520.56, P 5 0.08). An increase in hip extensor spasticity
correlated with a reduction in plasma insulin concentration at T30 (r 5 20.63, P 5 0.049). Additionally, an
increase in knee extensor spasticity associated with areduction in plasma insulin concentration at T60 (r 520.68, P 5 0.03). Spasticity did not seem to influenceinsulin sensitivity using the Matsuda and Defronzo
formula or the HOMA index. Knee extensor or flexor
spasticity did not seem to influence AUCs of plasma
glucose and insulin. However, after adjusting to total
FFM, extensor spasticity was negatively correlated to
AUCs of plasma glucose and insulin (r 5 20.64, P 50.04).
The outcomes of lipid profile are presented inTable 2. An increase in %FFM-total was associated witha reduction in plasma cholesterol (r 5 20.79; P 5 0.006)
and LDL (r 5 20.75; P 5 0.01). %FFM-trunk and leg was
associated with a reduction in plasma cholesterol (r 520.65, P 5 0.042 and r 5 20.64, P 5 0.045,
respectively) and LDL (r 5 20.59, P 5 0.06 and r 5
20.61, P 5 0.062, respectively). Partial correlations after
adjusting for oral baclofen are presented (Table 2).
Extensor spasticity was not related to any of theoutcomes of the lipid panel. However, knee extensor
spasticity was negatively related to LDL (r 5 20.56, P 5
0.049). After adjusting knee extensor spasticity for leg
FFM, this relationship was more pronounced (r 5 20.70,
P 5 0.025).
DISCUSSION
The tonic activity associated with spasticity may have aprotective effect against deterioration in body composition, energy expenditure, and metabolic profile inindividuals with motor complete SCI. Those withincreased spasticity in large muscle groups have less FM
and maintain high FFM. Spasticity per FFM is inversely
related to abdominal circumference. Moreover, spasticity
improves glucose homeostasis, insulin sensitivity, andlipid profile by primarily maintaining FFM. Additionally,
maintenance of FFM has been shown to positively
influence the RMR and hence the basal metabolic profile.

12

The findings support the observation that spasticity
may attenuate skeletal muscle atrophy early after
incomplete SCI and in people with chronic stroke(21,31). Spasticity could mimic isometric contraction or
low tension resistance training in maintaining lean mass.
Franzoi et al (32) showed that individuals with MAS 3
developed more torque output compared with thosewith MAS 1 or 2 or AB controls. Similar to aerobic orresistance training, the periodic tension of spasticity has
no preferential site specific on subcutaneous adipose
tissue. There were strong relationships between spasticity
and FM (total, trunk, gynoid) but not leg FM. In men, 20
weeks of aerobic training altered body fatness but theinduced fat loss does not deplete subcutaneous fat at a
specific site (33). In women, 5 weeks of resistancetraining caused increased muscle mass and reduction in
total fat mass, with no change in the thigh fat mass (34).
Previous reports documented a positive relation
between insulin growth factors and the body composition profile (35,36). It is plausible that spasticity
enhanced the expression of endogenous growth hormone and/or the potency of insulin growth factors (28),thus improving body composition profile. Growth
hormone response is blunted in individuals with chronic
SCI (37); whether spasticity enhances the quality ofgrowth hormone sensitivity needs to be further addressed. Another explanation is the ability of spastic
muscle to attenuate the shift in slow to fast muscle fibertransformation (25,26); slow fibers have a higher
mitochondrial concentration that may be responsible
for the increased fat oxidation observed in this study.
However, this may not be universal finding because hindlimb suspension in rats seems to reduce mitochondrial
volume in all fiber types (38).
Periodic recruitment of large skeletal muscle mass
could result in high energy expenditure and defend
against increase in FM after SCI. The involuntary activity
associated with spasticity may have resulted in increasing
the noncontractile ATP costs because of the activity of
Na+-K+-ATPase and Ca2+-ATPase. In accordance withrecent findings (39), spasticity was not directly related to
the RMR. However, successfully maintaining FFM resulted in increased RMR, respiratory exchange ratio, andsubstrate utilization, as documented by increased fat
oxidation. Therefore, therapeutic interventions that can

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2010attenuate skeletal muscle atrophy and promote hypertrophy are highly recommended to balance the disturbance in energy expenditure after SCI (40). Kneeextensor spasticity positively decreases the ratio between
FM to FFM in legs, trunk, and whole body. The increasein FM relative to FFM can be simply attenuated by
provoking spasticity in both lower extremities. The index
of FM/FFM in the arms represents a favorable norm that
could be used to determine the deviation in otherregional compartments, especially for those with low
cervical lesion and individuals with paraplegia.
Negative relationships were observed between spasticity and WC and abdominal circumference. Both WC
and abdominal circumference have been used asindicators of abdominal fat accumulation in healthy
and clinical populations. It would have been interesting
to measure visceral adiposity as determined by ultrasound or magnetic resonance imaging techniques.
However, circumferential measurements have been used
as an index for developing metabolic syndrome (41) andvisceral adiposity accumulation after SCI (42). The
relationships became negative after considering the%FM in the trunk and gynoid region, indicating that
increasing spasticity in lower extremities may contributeto reduce abdominal FM. The relationship was inversely
related after adjusting spasticity to FFM in the lower
extremities, suggesting that tension per unit FFM could
play a role in reducing abdominal fat. The speculation
was supported by the strong relationship between FFM
and RMR; this may indirectly contribute to caloric
expenditure and reduction in FM.
Skeletal muscle oxidative capacity is impaired inindividuals with SCI, predisposing them to further weightagain and developing type 2 diabetes mellitus (5,6). This
fact is confirmed by their low aerobic capacity and thehigh percentage of fast twitch fibers distributed in theparalyzed skeletal muscles (25,26). This may result in
impaired substrate utilization and lead to insulin resistance commonly seen in obese and elderly individuals(43). These findings may support the notion thatspasticity may enhance glucose uptake and improve
insulin sensitivity by maintaining FFM. In motor complete
SCI, spasticity could counteract the risk of developing
type II diabetes mellitus by increasing glucose uptake 3times higher compared with AB controls (22). It is
unclear how spasticity improves glucose homeostasis;
however, it has been suggested that spasticity could havea significant role through an insulin-independent mechanism (22). It is possible that spastic muscle fibers
triggers Ca++ release and stimulates translocation of
GLUT-4. Previously, we documented that spasticity could
help to reduce intramuscular fat, which is proven to
impair insulin sensitivity (9,21).
Persons with SCI have lower serum HDL cholesterollevels than AB controls (7,44). Serum total and LDLcholesterol, as well as TGs, were all higher in persons withparaplegia compared with controls because of distur-bances in the autonomic nervous system and low aerobic
capacity (44). This may impose an atherogenic risk ofdeveloping cardiovascular diseases and may explain thehigher incidence in SCI (,228%) compared with healthy
controls (4). Increasing physical activity improves thelipid profile and HDL in individuals with SCI (44,45,46).
Spasticity has been shown to benefit the overall pictureof lipid profile by reducing cholesterol, LDL, and TGs. The
findings may suggest that the use of spasticity as aninherent tool to exercise the paralyzed muscle may
improve the overall picture of lipid profile. This can beaccomplished by varying the dose of oral baclofen overthe course of treatment. Therefore, adjusting for oral
baclofen is crucial when managing spasticity in individuals with dyslipidemia.
The primary weakness of this study is the failure toaccount for baseline variations in body composition andmetabolic profile in this population. Body composition
may vary widely among individuals with SCI as a result of
the level of injury, years after injury, and extent ofphysical activity; therefore, it is unlikely that spasticity can
explain most of the variance in body composition after
SCI. The current observations about spasticity, bodycomposition, and metabolic profile are correlative, anddirect inferences are unlikely to be made. However, thestudy sheds light on factors that need to be further
addressed on the mechanistic role of spasticity after SCI,
lending credence to a longitudinal design to account forbaseline variations. This study followed strict inclusion
criteria to ensure a homogeneous small sample size.
Smoking, different antispasmodic medications, BMI .
30 kg/m2, and other chronic complications were primaryfactors that warranted exclusion from the study. Despite
quantifying spasticity over a 24-hour stay, the use of MAS
is considered a subjective tool, and objective measures
are highly recommended for future studies. Therefore, it
is crucial to evaluate extensor spasticity separated fromthe flexor one. The overall effects of lower extremity
spasticity (extensor + flexor) may not accurately reflect
the exact relationships on the examined variables,
because flexor spasticity may dilute the effects ofextensor spasticity (Figure 3).

CONCLUSION
Considering the well-established negative effects ofspasticity, this study showed evidence that individuals
with motor complete SCI may have desirable effects withregard to their body composition and metabolic profile
in response to spastic skeletal muscles. Spasticity may be
used as an exercise tool to develop periodical tension andprotect against other health-related complications. Potential clinical consideration should be given to balance
functional and quality of life issues related to muscle
spasticity with those related to soft tissue, metabolic, andlong-term cardiovascular outcomes.

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13

ACKNOWLEDGMENTS
We thank all our participants and Dr Denise Tate forproviding guidance during the course of the study.
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