Interesting Study on the Efficacy of Exercise to Improve ADL for Individuals Living with PD

Reviews
Parkinson’s Disease and Resistive Exercise: Rationale, Review,
and Recommendations
Michael J. Falvo, MS,1* Brian K. Schilling, PhD,2 and Gammon M. Earhart, PT, PhD1
1Movement Science Program, Washington University School of Medicine, St. Louis, Missouri, USA
2Exercise Neuromechanics Laboratory, University of Memphis, Memphis, Tennessee, USA
Abstract: Individuals with Parkinson’s disease (PD) are not
only burdened with disease-specific symptoms (i.e., bradykinesia,
rigidity, and tremor), but are also confronted with ageassociated
progressive loss of physical function, perhaps to a
greater extent than neurologically normal adults. Suggestions
for the inclusion of resistive exercise into treatment to attenuate
these symptoms were made over 10 years ago, yet very few
well controlled investigations are available. The objective of
this review is to establish a clear rationale for the efficacy of
resistance training in individuals with PD. Specifically, we
highlight musculoskeletal weakness and its relationship to
function as well as potential training-induced adaptive alterations
in the neuromuscular system. We also review the few
resistance training interventions currently available, but limit
this review to those investigations that provide a quantitative
exercise prescription. Finally, we recommend future lines of
inquiry warranting further attention and call to question the
rationale behind current exercise prescriptions. The absence of
reports contraindicating resistive exercise, the potential for
positive adaptation, and the noted benefits of resistance training
in other populations may provide support for its inclusion into
a treatment approach to PD. © 2007 Movement Disorder Society
Key words: Parkinson’s disease; resistive exercise; exercise
training; muscle strength.
Parkinson’s disease (PD), a progressive neurodegenerative
disorder, is manifested by a loss of dopaminergic
neurons from the substantia nigra pars compacta thereby
disrupting the basal ganglia circuitry. As a result, individuals
present with tremor, rigidity, progressive bradykinesia,
and postural instability.1 Currently, the primary
treatment option is administration of anti-Parkinson
medications (e.g., levodopa). Unfortunately, levodopa
loses effectiveness over time and leads to the appearance
and development of dyskinesias.2 Thereafter, patients
and health care providers may consider neurosurgical
options (i.e., deep brain stimulation). As these treatments
come with obvious risks and limitations, some authors
have suggested alternative treatment options to slow
disease progression and stimulate movement control.3
One such option, physical exercise, is generally accepted
to improve physical performance and activities of daily
living (ADL).4
Physical exercise has demonstrated a reduction in
mortality rate in individuals with PD5 and, albeit modestly,
a protective effect for PD risk.6 More immediate
effects include improved motor performance, cognitive
and functional ability.7 Specific to PD, these findings
may be a result of exercise stimulating the synthesis of
dopamine via increased serum calcium levels (for review,
see Sutoo and Akiyama 2003).8 Although this
hypothesis is derived from animal models, it is supported
by earlier work demonstrating a monotonic relationship
between dopamine activity and aerobic exercise workload.
9 While the precise mechanism has not yet been
identified, robust effects of exercise are well recognized
in this population and inclusion of exercise in the treatment
of PD is encouraged.
*Correspondence to: Michael Falvo, Washington University School
of Medicine, 4444 Forest Park Ave, Campus Box 8502, Saint Louis,
MO 63108. E-mail: mjfalvo@wustl.edu
Received 23 May 2007; Revised 3 July 2007; Accepted 4 July 2007
Published online 25 September 2007 in Wiley InterScience (www.
interscience.wiley.com). DOI: 10.1002/mds.21690
Movement Disorders
Vol. 23, No. 1, 2008, pp. 1-11
© 2007 Movement Disorder Society
1
Apart from disorder-induced symptoms of PD, individuals
are also confronted with the age-associated declines
in physical activity, strength, and quality of life.
This has led some investigators to denote PD as accelerated
aging.10,11 This term may appear appropriate in
light of reduced physical activity,12 greater muscle weakness,
13–15 and lower bone mineral density (BMD)16 when
compared to neurologically normal age-matched individuals.
Ultimately, these age- and disease-associated impairments
often confer a reduced quality of life.17 However,
the progression of these losses may be attenuated
through physical exercise, especially when the exercise
includes a resistive component.
Despite recommendations for the inclusion of strength
training into PD treatment more than 10 years ago,10,18
very few well-controlled investigations exist on this
topic. This is unfortunate as resistance training in neurologically
normal older adults has repeatedly been
shown to increase muscle mass, strength, and function,19
even in nonagenarians.20 The purpose of this review is to
reevaluate the rationale for resistance training, analyze
the existing literature, and suggest potential future
interventions.
RATIONALE FOR RESISTIVE EXERCISE
Muscle Weakness
Corcos et al.21 maintain that investigating muscle
strength in individuals with PD is essential as strength
influences the manner in which muscles are activated and
movement speed, and weakness can compromise ability
to perform ADLs. Both the former and latter have been
reviewed in detail elsewhere regarding normal aging,19
yet whether PD contributes uniquely to this process is
equivocal. Beradelli et al.22 identified muscle weakness
as a secondary cause of bradykinesia due to increasing
evidence demonstrating individuals with PD to be
weaker than neurologically normal adults in a variety of
muscle groups,23-25 and muscle weakness has been suggested
to be a primary symptom of PD.26 In addition,
muscle weakness is recognized as one of the factors
contributing to postural instability.27 Despite these suggestions,
some ambiguity remains as to whether individuals
with PD are actually weaker than neurologically
normal adults due in part to methodological issues, disease
severity, and medication status. Medication status
(i.e., ON or OFF) is of considerable importance as
strength is reduced during periods of withdrawal.21,27,28
Pedersen and Oberg28 have suggested that strength measurements
may be an appropriate evaluation method of
pharmacological therapy as reductions in strength were
found to be correlated with disability changes following
withdrawal of medication.
Strength may also be delineated into time-related components.
It appears that longer latencies are necessary for
muscle force production and relaxation in individuals
with PD.14,21 These obvious time-related decrements of
force production appear to be related to the pathophysiology
of bradykinesia and have led some researchers to
stress the importance of the rate of force development for
monitoring motor control in PD.14 Maximal or absolute
strength has been shown to be significantly correlated
with rate of force development in older adults29 and
individuals with PD,21 but this has not been noted in all
investigations.14 Interestingly, when controlling for
strength, no differences were observed in contraction
time of the elbow flexors between individuals with PD
and neurologically normal adults.30 Presumably, if this
relationship between strength and speed is robust and
trainable, responses to postural disturbances (e.g., balance)
and functional capacity may be improved. Some
authors have suggested that maximal strength31 and the
rate of force production32 of the lower extremities is
critical during a period of compromised balance,
whereby sufficient force is necessary to orient the body’s
center of mass over the base of support in a short period
of time. Elaboration of muscle weakness as it relates to
PD is discussed below (“Cross-Sectional Investigations”)
and presented in Table 1.
Central Manifestations
Cortical afferents arrive at the striatum (caudate and
putamen) in anatomically distinct locations, thereby creating
unique circuits.33 In the basal ganglia-thalamocortical
motor circuit, afferents from motor regions of cortex
(M1, pre-motor, supplementary, and somatosensory) terminate
on the striatum (caudate and putamen), which
also receives dopaminergic innervation from the substantia
nigra pars compacta.34 Inhibitory projections from the
striatum terminate on the globus pallidus external (indirect
pathway) and internal (direct pathway) segments,
which in turn sends inhibitory projections to the ventral
anterior and lateral thalamus. Inhibitory outputs from the
globus pallidus internal segment have been suggested to
serve two distinct functions: (1) focused selection of the
desired movement and (2) inhibition of competing
movements.35
Functional anatomists suggest motor cortices are not
fully activated secondary to abnormal drive from the
basal ganglia to the thalamus, thereby impeding the
facilitation of desired movement.36 This impaired cortical
activation can lead to inability to sufficiently activate
motoneuron pools, thereby affecting recruitment and dis-
2 M.J. FALVO ET AL.
Movement Disorders, Vol. 23, No. 1, 2008
charge rate.18 This may ultimately result in reduced neural
drive (i.e., EMG amplitude), and general muscle
weakness.10 Ultimately, these clinical findings may contribute
to the progressive deterioration in function
observed in these patients. Consistent with these reports
are electroencephalographic recordings (e.g., Bereitschaftspotential)
reporting underactivation of the cortex
in areas ascribable to movement preparation, planning,
and execution.37 Dick et al.37 also demonstrated that
differences between patients and neurologically normal
adults were dependent on dopaminergic function. Therefore,
it appears that peripheral manifestations (i.e., decreased
EMG activity) are centrally-mediated, which
may contribute to diminished muscle strength. These
observations, in concert with the noted increase in
strength due to medication,38 demonstrate that weakness
is clearly due at least in part to central nervous system
function.26
Following short-term strength training, significant
gains in maximal force production occur without concomitant
muscle hypertrophy. It is generally agreed that
neural adaptations are responsible for this enhancement,
which manifests as increased amplitude of the surface
electromyographic signal.39 Griffin and Cafarelli40 suggest
this increase in neural drive, along with lower recruitment
thresholds observed subsequent to training,
may reflect adaptations at the level of the central nervous
system. To quantify this increase in neural drive, some
investigators superimpose a supramaximal electrical
pulse to contracting muscle (i.e. interpolated twitch) to
determine whether the motoneuron pool has been sufficiently
activated to produce maximal force.41 More recent
techniques, such as transcranial magnetic stimulation
(TMS), have also been used to quantify voluntary
activation.42 Both interpolated twitch and TMS methods
may be useful to investigate the potential for chronic
adaptation induced by resistance training43 as well as
estimate how well the brain is able to drive muscle
contraction.41 However, TMS methods are unable to
definitively establish whether resistance training is capable
of affecting the functional organization of the cerebral
cortex,44 despite the well established changes induced
via motor learning.45
Evoked spinal reflexes, Hoffman-reflex (H-reflex) and
V-wave, have also been used following resistance training
to assess the excitability of the
-motoneurons and
the magnitude of output from descending central pathways,
respectively.46 Following 14 weeks of strength
training, Aaagard et al.46 demonstrated parallel increases
in isometric strength and H-reflex and V-wave amplitudes,
indicative of enhanced supraspinal drive and motoneuron
excitability. Additional indirect lines of evidence
pointing toward centrally mediated neural
adaptations have also been demonstrated in the literature,
including reductions in agonist-antagonist coactivation,47
and cross-education (i.e., transfer of unilateral training
effects to the contralateral limb).48 It remains to be
established whether these adaptations are attainable in
individuals with PD. In brief, resistance training may be
of therapeutic value to individuals with PD to enhance
neural drive to the agonist as well as decrease coactivation,
both contributing to improved strength and movement
control.
Bone Health
A recent review49 identified PD as a secondary cause
for osteoporosis. Several investigations have associated
PD with low BMD,16 but exist with noteworthy limitations
including selection bias, reporting only single BMD
sites, and not controlling for influencing external factors.
16 Perhaps the greatest support to date is derived
from the Osteoporotic Fractures in Men Study Group
(MrOS), where lower BMD at the hip and spine was
associated with PD irrespective of physical activity and
neuromuscular function.16 However, PD status was
based on self-report questionnaires. Authors from the
MrOS promote the potential to lower fracture risk in
persons with PD via physical training aimed at reducing
bone loss and/or promoting favorable bone augmentation.
Consistent with this approach, loads applied to the
bone via the muscular system in addition to loading the
axial skeleton, which can be accomplished through resistive
exercise, have direct effects on bone formation
and remodeling, a hallmark of Wolff’s Law.50
Some investigations have reported low BMD in individuals
with PD at the hip51 and low back,52 which may
be related to the three-fold greater incidence of hip
fracture in PD patients compared to age- and sexmatched
controls.53 This high incidence rate of fracture
is of serious concern due to its association with disability,
pain, and especially mortality.54 This concern is
amplified due to previous reports from Sato et al. demonstrating
vitamin D deficiency (i.e., 25-hydroxyvitamin
D levels less than 10 ng/mL) in individuals with PD,
which may induce conditions of hyperparathyroidism
and exacerbate loss of BMD.55 Compensatory hyperparathyroidism
is likely manifested by a lack of exposure
to sunlight. This is consistent with previous reports of
individuals with PD performing less physical activity,12
especially after the initial appearance of symptoms.56
Subsequent well-controlled investigations by Sato et
al.57,58 demonstrated the efficacy of administering biophosphonates
(2.5–5 mg/day) and ergocalciferol (1000
PARKINSONS DISEASE AND RESISTIVE EXERCISE 3
Movement Disorders, Vol. 23, No. 1, 2008
IU/day) for 2 years in elderly men and women with PD
to improve BMD and reduce hip fracture risk.
The American College of Sports Medicine (ACSM)
maintains the efficacy of weight-bearing exercise to promote
bone health across the lifespan,59 and weight-bearing
physical activity programs are widely used in the
prevention and treatment of osteoporosis.60 Several reviews
and meta-analyses in regards to neurologically
normal older adults are available on the utility of resistive
exercise.61–63 In brief, it is intuitive and encouraged
to pursue progressive resistive exercise as a viable treatment
to improve bone parameters, but an optimal strategy
remains to be determined. Presumably, individuals
with PD may stand to derive equal benefit from resistive
exercise. Moreover, the combination of pharmacotherapy
(e.g., biophosphonates, vitamin D) and resistive exercise
may confer an even greater benefit for individuals
with PD. However, to the knowledge of these authors,
such investigations (i.e., combined treatment and/or resistance
training alone) are surprisingly absent from the
literature regarding bone health outcomes in individuals
with PD.
Relationship to Function
Navigating stairs and rising from a chair are performed
at an effort level close to maximal force production
capabilities in healthy older adults,64 likely due to
substantially lower maximum strength in this group. This
group also has inefficient activation (e.g., increased drive
to both agonist and antagonist), which likely contributes
to fatigue, thereby limiting ADLs. Although Hortobagyi
et al.64 only considered neurologically normal adults, the
altered activation patterns they observed have been reported
in PD.10 In addition, fatigue is more pronounced
in patients with poorer functional capacity,65 and is considered
one of the three worst self-reported symptoms of
PD.66,67 These myoelectric disturbances and altered
bioenergetics are likely associated with muscle weakness
in this population, collectively affecting ADLs. As most
ADLs involve the lower extremities (i.e., chair-rise, ambulation),
weakness of this musculature is of considerable
interest, and may also compromise the ability to
mount a defense against a postural disturbance.31,32
Rising from a chair is an objective measurement used
to evaluate functional limitations and is suggested to be
a major factor in independence and quality of life in
individuals with PD.68 Sit-to-stand performance in this
population is impaired, particularly the time necessary to
transition from forward flexion to an extension direction.
69 Further, biomechanical analysis of this task reveals
reduced torques and rate of force development at
the hip, knee, and ankle as compared to controls.69 Other
investigators have reported a correlation between sit-tostand
time and hip strength (r  0.71),13 and bilateral
leg extension strength (r  0.63)14 in individuals with
PD. Presumably, enhancing the maximal strength and
rate of force production in these patients may improve
sit-to-stand time. This has recently been observed in
consecutive sit-to-stands (e.g., 11% improvement) following
12 weeks of moderate resistance exercise and
creatine monohydrate supplementation in individuals
with PD (See Table 2).70
Gait disturbances are prevalent in PD and are one of
the most critical motor impairments71 as they contribute
to falls, loss of independence, and institutionalization.72
Individuals with PD generally have slower gait velocity,
increased stride variability, and increased double support
time.73,74 Increased time spent in double support is associated
with increased falls in the elderly, and it may be
that those with poor postural stability use increased double
support as a compensatory mechanism to help avoid
falls.75 Other features of parkinsonian gait, specifically
festination and freezing, may also predispose individuals
to falls.76 Therefore, a clinical assessment of gait is
critically important to the welfare of the patient, particularly
as disease severity progresses.
Scandalis et al.73 stated that strength training is generally
assumed to improve gait, which has been observed
in neurologically normal older adults,77 yet few investigations
are available pertaining to PD. The linear relationship
between leg strength and gait speed has been
well defined in respect to healthy older men and women,
with composite leg strength explaining 17% of the variance
in gait speed.78 Interestingly, nonlinear regression
analysis demonstrated that in those with less strength it
explained a greater proportion of variance (22%). Recently,
Nallegowda et al.27 demonstrated strength of the
ankle, hip, and trunk to be positively correlated with gait
velocity in individuals with PD. Similar to neurologically
normal adults, ankle strength explained 15% of the variance
in gait speed in individuals with PD while ON
medication.27
Scandalis et al.73 showed that a simple resistive exercise
program increased gait speed in persons with PD, so
much so that there was no significant difference in gait
speed between persons with PD and controls at the end of
the 8-week study. In simple gait tasks, the role of
strength and utility of strength training appear to be
evident. Even in more complex tasks, such as gait while
negotiating obstacles, 24 weeks of progressive resistance
training demonstrated 5–15% improvements in stride
velocity during obstacle crossing in healthy older adults.
Such results were concomitant with strength improve-
4 M.J. FALVO ET AL.
Movement Disorders, Vol. 23, No. 1, 2008
ments of 197–285%.79 These relationships remain to be
determined in PD.
CROSS-SECTIONAL INVESTIGATIONS
Several descriptive studies are available that analyze
force production capabilities in individuals with
PD.21,26,80,81 These studies unfortunately do not compare
persons with PD to neurologically normal age- and sexmatched
controls. There appears to be a general agreement
that the rate of force production is decreased in
individuals with PD, consistent with bradykinesia. To
understand the normal effects of aging, comparison with
neurologically normal adults is important and is presented
in Table 1. Although previous reports have demonstrated
weakness to be more pronounced in the more
affected limb of individuals with marked laterality of
symptoms,26,80 this was not observed for the investigations
presented in Table 1.13–15,27,82–84 Observed interlimb
differences appear to be velocity-dependent, such
that strength differentials between the two sides are more
pronounced at greater velocities.81 Pedersen et al.83,84
compared high velocity isokinetic measurements of the
dorsiflexors between individuals with PD and controls,
but no delineation for more or less affected limbs was
made.
From Table 1, individuals with PD appear weaker and
slower than neurologically normal adults across a spectrum
of testing modalities (i.e., isometric, isokinetic,
isotonic) and across muscle groups of the upper- and
lower-extremities. Interestingly, Pedersen et al.83,84 examined
ankle dorsiflexion strength during concentric and
eccentric (i.e., shortening or lengthening) muscle actions
separately. Torques for both action types were measured
at five84 or three83 different velocity settings. As expected,
power (Nm/s) decreased proportionally with increasing
movement velocity for concentric actions (30°/
s  1,882, 120°/s  918, 180°/s  647), which has been
supported elsewhere.80 However, this relationship was
not observed for eccentric actions as power remained
constant (30°/s  2,480, 120°/s  2,628, 180°/s 
2,833). These relationships were also demonstrated in
the companion study84 and earlier work by the same
authors.28 Despite the preservation of eccentric torque, or
power, individuals with PD remained weaker than controls.
This finding has previously been demonstrated in
neurologically normal adults whereby eccentric strength
appears to be less influenced by aging.85 These authors
imply that a resistive exercise program composed of a
large eccentric component may provide a unique treatment
option. Eccentrically biased exercise may be a
viable alternative given the muscle can withstand greater
forces while lengthening rather than shortening, thus
performing more work (work  force  distance). The
ability to produce more work via eccentric training rather
than concentric training has been recognized previously,86
and has recently been exploited in individuals with PD.87
RESISTANCE TRAINING INTERVENTIONS
Research syntheses evaluating the utility of physical
therapy7 or physical exercise4 as an appropriate supplement
to pharmacological treatment have been documented
previously and generally support their inclusion.
However, two comprehensive reviews88,89 concluded
there is insufficient evidence to support or refute any
form of physiotherapy. These authors present a broad
definition of physiotherapy that includes a variety of
treatment techniques that may or may not include resistive
exercise. Additionally, many investigations fail to
adequately quantify the training intervention, which
makes interpretation of resistive exercise studies extremely
difficult. Said investigations utilize descriptors
such as “strengthening exercises” or “exercises for improving
strength ” to describe the protocol employed.90,91
This brevity ultimately clouds the interpretation of findings
and does not allow for meaningful comparison. To
circumvent these limitations, attention must be paid to
the acute variables that comprise a resistive exercise
prescription (e.g., mode, volume, temporal expression of
force, multi- vs. single-joint exercises, rest periods, etc.).
Herein, we review those investigations that provide a
detailed exercise prescription and do not include those
considered ambiguous or those that included only subjective
outcomes.90-93 To the knowledge of these authors,
only five well controlled clinical trials are available at the
time of this review, and are presented in Table 2.
Postural disturbance or compromised balance in general
is considered an intrinsic risk factor for falling in
Parkinson’s disease.94 In attempts to improve postural
stability, Toole et al.31 and Hirsch et al.95 combined 10
weeks of lower extremity progressive resistance training
(PRT) and exercises performed on unstable surfaces to
promote balance and strength. Although these investigations
were similar, Toole et al.31 randomly assigned
patients to treatment PRT and balance exercises (n  4)
or control (no-exercise; n  3) groups, whereas Hirsch et
al. (2003) assigned subjects to treatment (PRT/balance;
n  9) and quasi-control (balance only; n  6) groups.
Exercise volume was greater for Toole et al.31 than
Hirsch et al.95 (90 repetitions per muscle group per week
versus 36 reps/week), but were performed at a lower
intensity (60% of 4 repetition maximum [RM] versus
80% of 4RM). As higher loads are widely known to
foster the greatest training effect,96 it is not surprising
that the treatment group of Hirsch et al.95 experienced
PARKINSONS DISEASE AND RESISTIVE EXERCISE 5
Movement Disorders, Vol. 23, No. 1, 2008
large composite strength gains (52%) compared to modest
increases (7%) for Toole et al.31 It should be noted
that Toole et al.31 used isokinetic strength testing, which
is not specific to the isotonic training, and may have
contributed to moderate training effects.97 In general, it
appears that PRT was effective in improving strength
and balance in these experiments and gains were still
present 4 weeks after cessation of exercise.95 The investigation
used by Hirsch et al. in Ref. 95 is the only
investigation to monitor detraining effects (e.g., knee
flexors/extensors) following an intervention in this
population.
In the only clinical intervention to include age- and
sex-matched healthy controls, Scandalis et al.73 trained
TABLE 1. Cross-sectional investigations (PD and control comparisons)
Reference Subjects
Muscles tested/measurement
device Results Comments
Paasuke et al., 200215 1) 14F PD (72.6 yrs, 1-3
HY)
2) 12F Con (72.8 yrs)
Knee extensors; UL
Isometric knee extension; ON
(knee  90°, hip  110°)
Analyzed best of three trials
PD had 2 MF, 2 RFD
than controls
No difference for relative
MF
1) PD patients more
deficient in rate rather
than absolute force
2) RFD reflected in longer
chair rise time
3) No strength asymmetry
Paasuke et al., 200414 1) 12F PD (74.3 yrs, 1-3
HY)
2) 16F Con (71.7 yrs)
Leg extensors; UL and BL
Isometric leg extension; ON
(knee  120°, hip  110°,
ankle  60°)
Analyzed best of three trials
PD had 2 BL MF, 2
relative MF, 2 RFD than
controls
1) PD patients were
generally weaker (rate
and max)
2) Longer chair rise time
3) No strength asymmetry
Koller and Kase, 198682 1) 21M PD (62.5 yrs, 1.2
HY)
2) 21M Con (65.2 yrs)
Wrist, arm, knee; BL
Isotonic measurement on
isokinetic device (5 rev)
Three patients did not take
medication
All other patients were ON
PD had 2 BL strength for
all muscles than controls
PD had 1 endurance in
knee, L wrist, and L arm
than controls
1) PD patients had average
3.1 yrs of symptoms, yet
still were weaker
2) Greater endurance is
likely a function of the
reduced load
3) No strength asymmetry
Inkster et al., 200313 1) 10M PD (64.1 yrs, 2.1
HY)
2) 10M Con (65.5 yrs)
Hip (BL) and knee (UL)
extensors
Isokinetic hip and knee
extension; ON and OFF
(45°/s)
PD had 2 hip and knee MF
(torque) than controls
1) No difference ON and
OFF for knee torque,
but not hip torque
2) Hip torque explained
50-64% variance in sit-tostand
times
3) No strength asymmetry
Pedersen et al., 199784 1) 14M, 11F PD (63.7
yrs, 1-3 HY)
Ankle dorsiflexors; UL
Isokinetic ankle dorsiflexion;
medication? (0, 15, 30,
120, 180°/s)
PD had 2 concentric torque
at all velocities than
controls
1) Eccentric torque is well
preserved in PD,
especially for women

2) 19M, 18F Con (60.4
yrs)
Only men had 2 eccentric
torque than controls
Pedersen et al., 199783 1) 7M, 3F PD (62.3 yrs,
1-3 HY)
2) 7M, 4F Con (66.0 yrs)
Ankle dorsiflexors; UL
Isokinetic ankle dorsiflexion;
ON
Concentric, eccentric, SSC;
(30, 120, 180°/s)
EMG of anterior tibialis and
gastrocnemius
PD had 2 torque for all
velocities and muscle
action types than controls
PD had 1 iEMG for all
velocities and conditions
except SSC at faster
velocities than controls
1) PD had lower
contraction efficiency
2) Authors suggest
eccentric torque might
be important for
dynamic movements
Nallegowda et al., 200427 1) 25M, 5F PD (57.7 yrs,
2.7 HY*) HY*  OFF
2) 25M, 5F Con (agematched)
Ankle dorsi- and plantarflexion;
UL
Hip flexion and extension
Trunk flexion and extension
(90, 120, 150 °/s)
ON and OFF testing
Only concentric torque
reported
PD had 2 torque for all
measures than controls
(ON and OFF) except left
ankle dorsiflexion and
trunk flexion (ON was NS)
PD ON had 1 torque for all
measures except right ankle
plantarflexion (120°) and
dorsiflexion (90°)
1) PD were weaker at
ankle, hip, and trunk for
most all measures,
regardless of medication
2) Ankle strength for PD
correlated with gait
velocity
3) Authors suggest muscle
weakness is a factor for
postural instability
M male, F  female, Con  neurologically normal, HY  Hoehn and Yahr stage, UL  unilateral, BL  bilateral, MF  maximal force, RFD 
rate of force development, 2  lower, 1  greater, ON  patients had taken parkinsonian medication, OFF  patients were on an overnight
withdrawal of medication, (?)  unknown, NS  not significant.
6 M.J. FALVO ET AL.
Movement Disorders, Vol. 23, No. 1, 2008
controls and individuals with PD for 16 sessions. Interestingly,
no differences were evident between the groups
at baseline or after 8 weeks of training for leg curl,
extension, press, and toe raise performance. As both
groups improved total exercise volume (repetitions 
load) with training, authors suggest that these findings
(e.g., no differences at post-testing) demonstrate that
individuals with PD can experience improvements similar
to those of neurologically normal controls. These
findings should be interpreted cautiously as groups were
unequal in size (PD  14, control  6), the training
intensity was moderate, and individuals with PD were
likely at an early-stage of their disease progression
(Hoehn and Yahr average  2.5). This study also analyzed
gait and observed group differences for stride
length and hip velocity that were shorter and slower in
individuals with PD at baseline, respectively. After training,
only those with PD significantly increased stride
length (14.4%) and hip velocity (7.5%). Hip velocity
after training for individuals with PD was not different
from that of controls. Although this study demonstrated
moderate training effects on gait and strength, it must be
considered in light of the training protocol which consisted
of very few sessions (e.g., 16 sessions) of lightmoderate
intensity. These improvements further support
the significant positive correlation observed between ankle
strength and gait velocity in individuals with PD
without any intervention.27