Special Populations

The Special Populations Column provides personal

trainers who work with apparently healthy or medically
cleared special populations with scientifically supported
background information.

COLUMN EDITOR: Peter Ronai, MS, RCEP, CSCS*D,

NSCA-CPT

Parkinsons Disease:
Epidemiology,
Pathophysiology, and
Exercise Intervention
Lance M. Bollinger, MA,1 Celsi E. Cowan, BS,2 and Thomas P. LaFontaine, PhD3
1
Kinesiology Department, East Carolina University, Greenville, North Carolina; 2Department of Nutrition and Exercise
Physiology, University of Missouri, Columbia, Missouri; and 3University of Missouri, Columbia, Missouri

SUMMARY Common clinical symptoms of PD inc- consciousness, and antidepressant

PARKINSONS DISEASE (PD) IS A
PROGRESSIVE NEURODEGENER-
ATIVE DISEASE THAT IS ACCOM-
PANIED BY SEVERE MOTOR
SYMPTOMS THAT PRESENT
FUNCTIONAL LIMITATIONS. EXER-
CISE HAS BEEN SHOWN TO POS-
ITIVELY MODIFY PD SYMPTOMS
AND IMPROVE QUALITY OF LIFE
FOR PERSONS WITH PD.
arkinsons disease (PD) is a rela-
lude tremors, bradykinesis (slow speed
of movement), rigidity, and impaired
postural reflexes (14,19). This is typi-
cally because of decreased or altered
neurotransmission. Although PD is
a progressive, degenerative neurological
disease, evidence suggests that exercise
intervention may help improve stre-
ngth, balance, gait, and overall func-
tional status. The aim of this article is
to discuss the epidemiology, patho-
physiology, and exercise considerations
for persons with PD. Specific exercise
drug use along with family history
are all positively related to PD (6).
One study found that first-degree
relatives of PD patients demonstrated
a 3.5-fold increase in odds of devel-
oping PD (18). Recent evidence has
linked dysregulation of several genes
to the development of PD (8). This
suggests that, PD may be, at least in
part, a heritable disease. Additional
proposed causes of PD include mito-
chondrial dysfunction and/or reac-

P tively common neurodegenera-

tive disease. It is estimated that
PD affects approximately 340,000
adults in the United States and this
number is expected to nearly double
(610,000 cases) by the year 2030 (7). In
Japan, for example, PD prevalence
increased approximately 12% from
1980 to 2004 (23). This suggests that
as the population ages, PD prevalence
is likely to increase. Indeed, age ap-
pears to be the leading risk factor for
developing PD.
recommendations are addressed in the
accompanying One-on-One column.
EPIDEMIOLOGY
Although the specific cause(s) of PD
are not known, incidence increases
with age, especially after 50 years
(22). Both genders and all ethnic
groups appear to be susceptible to
PD; however, PD is approximately 2
times higher in men than women (22).
Environmental risk factors such as
pesticide exposure, repeated loss of
tive oxygen species formation (15).
Interestingly, many of the dysregu-
lated genes involved in the develop-
ment of PD are also involved in
mitochondrial regulation (15).
The 4 principal symptoms of PD are
resting tremor, bradykinesis, rigidity,
and decreased postural reflexes. Sec-
ondary motor symptoms include
shuffling gait, festination, freezing,
dystonia, hypomimia, dysarthria, dys-
phagia, sialorrhea, micrographia, and
glabellar reflex. The definitions

50 VOLUME 34 | NUMBER 2 | APRIL 2012 Copyright National Strength and Conditioning Association
associated with Parkinsons disease Table 1
are listed below: Common motor and nonmotor symptoms of Parkinsons disease (14)
Akathisiarestless sensation of lower
extremities (also known as restless Symptoms Description
leg syndrome). Motor
Cachexiaextreme weight loss, espe-
cially of skeletal muscles. Posture Forward leaning at waist
Dysarthriapoor articulation. Instability
Dyskinesisirregular movement pat-
terns due to difficulty performing Gait Decreased step length
voluntary muscle contractions. Decreased foot clearance
Dysphagiadifficulty swallowing.
Dystoniaabnormal tonicity of mus- Shuffling of feet
cle tissues resulting in unnatural Festination
positions on head and/or limbs.
Festinationshort rapid steps, usu- Freezing-inability to initiate or sudden stoppage of gait
ally in an attempt to maintain Tremors Postural Back and forth oscillation while standing
balance due to excess trunk flexion.
Resting Pill rolling between thumb and forefinger
Freezing (motor block)involuntary
sudden loss of or inability to initiate Intention Oscillation of limb during movement
movement.
Bradykinesis Decreased speed of movement
Glabellar reflexpersistent blinking
in response to repetitive tapping on Decreased range of motion
forehead.
Decreased coordination
Hypomimiareduced or loss of facial
expressions. Rigidity Involuntary muscular resistance to external forces
Micrographiaprogressively smaller independent of speed
handwriting. Nonmotor
Sialorrheaexcessive salivation.
Additionally, PD patients often suffer Neuropsyschotic Mood disorders
from nonmotor symptoms such as Anxiety
neuropsychiatric, cognitive impair-
ment, autonomic, sensory, and sleep Depression
disorders. Both motor and nonmotor Cognitive decline
symptoms can present significant func-
tional limitations that worsen with Dementia
disease stage. Common symptoms Autonomic Gastrointestinal problems
and related functional limitations of
Urinary dysfunction
PD can be found in Table 1. It should
also be noted that PD may be acc- Orthostatic hypotension
ompanied by other age-associated
Dysphagia
conditions, such as hypertension, car-
diovascular disease, and/or arthritis. Sensory Pain
Often the initial symptoms are rela- Akathisia
tively minor and may be disregarded as
Loss of smell
due to aging. This can delay a correct
diagnosis by as much as 23 years (16). Sleep Difficulty falling asleep or maintaining sleep
Additionally, because PD is a progres- Apnea
sive disease, diagnosis is not sufficient
to indicate severity of disease. Several
tools have been proposed to classify degree of subjectivity, they can be very PATHOPHYSIOLOGY AND
the stage of the disease. Perhaps, the useful in determining functional status PHARMACOLOGY
most common tool used is the Hoehn of the patient and provide some Although PD affects numerous areas of
and Yahr Staging Scale (13) (Table 2). information as to progression of the the central nervous system, the primary
Although these tools involve some disease. brain areas affected are the basal ganglia,

Strength and Conditioning Journal | www.nsca-lift.org 51

Special Populations

thalamus, and reticular formation (19),
all of which are involved in motor
control. The substantia nigra, located
within the basal ganglia, is particularly
sensitive to the pathological processes
involved in PD. The balance between
the neurotransmitters dopamine and
acetylcholine is critical for coordinated
motor control (4). In PD, dopaminergic
cells within the basal ganglia are
targeted for degradation. This results
in an altered balance of these neuro-
transmitters such that dopamine is
decreased, causing a relative increase
in acetylcholine. The altered neurotrans-
mitter balance results in the abnormal
motor control patterns observed in PD.
Pharmacological treatment of PD can
relieve many of the motor symptoms.
Typically, levodopa (L-DOPA) is pre-
scribed to compensate for the decreased
dopamine associated with PD. Levodopa
is structurally similar to dopamine and
stimulates the dopamine receptor to
decrease symptoms. This has consistently
proven to be the most effective treatment
for PD (16). However, as tolerance for L-
DOPA develops, symptoms can return
during off periods. The most common
time for this to occur is the period
between doses. Additional treatments
include anticholinergics, monoamine ox-
idase-B, and catechol-O-methyl trans-
ferase inhibitors. These drugs function to
decrease acetylcholine, slow the degra-
dation of dopamine, and slow the
degradation of L-DOPA, respectively.
Common medications used in the treat-
ment of PD can be found in Table 3.
EXERCISE INTERVENTION
Although exercise does not alter
the disease process, it has been shown
to improve movement and physical
capacity. Specifically, exercise appears
to positively modify PD by increasing
range of motion (ROM), decreasing
rigidity, increasing muscular strength,
improving activities of daily living
(ADLs), and reducing comorbidities.
Performance of specific exercise techni-
ques is a function of the symptoms of
the individual, functional limitations,
and stage of disease. During early stages
of PD (stages 12 on the Hoehn and
Yahr Scale), patients may present with
very few limitations. However, during
later stages, functional limitations may
present significant difficulty with both
resistance training (RT) and aerobic
training (AT). Exercise prescription
should focus on improving flexibility,
muscular strength and endurance, and
cardiorespiratory conditioning. Addi-
tionally, emphasizing functional training

Table 2
Hoehn and Yahr staging of Parkinsons disease
Stage Original scale (13) Modified scale [adapted from Protas and Stanley (19)]

1 Unilateral symptoms only Unilateral signs and symptoms

Symptoms mild
Inconvenient but not disabling symptoms
Noticeable changes in posture, gait, facial expressions
2 Bilateral symptoms Bilateral symptoms
No impairment of balance Minimal disability
Posture and gait affected
3 Balance impairment Bradykinesis evident
Mild to moderate disease Equilibrium compromised with walking and standing
Physically independent Moderately severe generalized dysfunction
4 Severe disability but still able to walk or stand unassisted Severe symptoms
Limited walking ability
Rigidity and bradykinesis apparent
Loss of independence
Tremor present (may be less severe than earlier stages)
5 Needing a wheelchair or bedridden unless assisted Cachexia
Completely invalid
Unable to stand or walk
Constant nursing care required

52 VOLUME 34 | NUMBER 2 | APRIL 2012

 Table 3
Common medications for treatment of Parkinsons disease

Class Generic name Trade name Mechanism of action Side effects

Dopaminergics Levodopa Sinemet Converted to Hypotension
dopamine in brain
Bromocriptine Parlodel (levodopa); stimulate Nausea
Pramipexole Mirapex dopamine receptors within Dyskinesis
brain (all others)
Ropinirole Requip Edema
on/off times
Anticholinergics Benztropine Cogentin Decrease Confusion
neurotransmission because
of decreased acetylcholine Hallucinations
Trihexyphenidyl Artane to alleviate tremors Nausea
Procyclidine Nervousness
Blurred vision
Monoamine oxidase-B inhibitors Selegiline (deprenyl) Eldepryl Prevent degradation Dyskinesis
of dopamine and levodopa
to effectively increase Joint/back pain
Rasagiline Azilect dopamine Agitation insomnia

Catechol-O-methyl transferase Entacapone Comtan Prevent degradation of Abdominal pain

inhibitors levodopa
Back pain
Constipation
Tolcapone Tasmar Nausea
Diarrhea
Bloody urine
Liver failure

and motor control can improve balance,
coordination, performance of ADLs,
and independence.
FLEXIBILITY
Flexibility training can effectively
increase ROM and reduce rigidity.
Rigidity, involuntary muscular resis-
tance to external force, can present
a barrier to flexibility exercises. Slow
static stretches have been shown to
increase flexibility in persons with PD
(20) and should be the basis for flexibility
training. Emphasis should be placed on
upper-body and trunk training because
PD initially affects these areas.
RESISTANCE TRAINING
RT has been demonstrated to improve
muscular strength in persons with PD.
Even high-intensity eccentric exercise
can be a safe and effective means of
increasing muscular strength in persons
with PD (stage 13) (5). Additionally,
combining RT with balance training is
more effective for improving balance
than balance training alone (12). It
should be noted that muscle strength
is inversely related to movement speed
in persons with PD (17). Therefore, it is
likely that exercise at lower velocities
may elicit greater muscular recruitment
in these persons, whereas high-velocity
RT may increase speed-specific muscle
strength. When compared with tradi-
tional low-velocity RT, high-velocity
RT provides comparable strength gains
and improves functional performance to
a greater extent in older men (2). High-
velocity training involves performing
resistance exercises at 60% of 1
repetition maximum, with 1 second
each of concentric and eccentric phases.
AEROBIC CONDITIONING
Like RT, the effects of AT on PD have
received little attention. Peak bicycle
ergometer oxygen uptake appears to be
similar among persons with PD (stages
13) and healthy age-matched controls
(21). This suggests PD does not in-
herently limit aerobic capacity. It is
important to consider functional limi-
tations of PD when prescribing AT.
Although treadmill exercise has been
shown to improve gait mechanics (11),
walking speed (3), and aerobic capacity
(1) of persons with PD, this may be
unsafe for individuals with advanced PD
(stage 3 or greater). For these persons,
other means of AT, such as bicycle and
arm ergometry, may be safer modes.

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Special Populations
FUNCTIONAL TRAINING
Functional training, such as balance
and gait exercises, may improve the
ability to perform ADLs. Compared
with controls, persons with PD par-
ticipating in physical therapy empha-
sizing functional training were
significantly better able to perform
ADLs (9). Balance exercise has been
shown to improve both sensory orien-
tation and latency to fall in persons
with PD, particularly when combined
with RT as discussed earlier (12).
Additionally, external cueing, such as
from a metronome, can be an effective
means of improving stride frequency in
persons with PD (10). Other functional
exercises, for example, unloaded ROM
exercises, may improve ability to
perform daily tasks, such as dressing.
SUMMARY
PD presents a complex array of motor
and nonmotor limitations to patients.
Exercise intervention can be an effective
means of improving functional ability,
slowing disease symptoms, and improv-
ing independence. Exercise professio-
nals should obtain medical clearance
and maintain open communication
with other members of the clients
medical team. Additionally, being aware
of the challenges presented by PD and
being familiar with strategies to effec-
tively implement exercise may improve
quality of life for PD patients.
Lance M. Bollinger is pursuing a PhD
in Bioenergetics and Exercise Science at
East Carolina University.
Celsi E. Cowan is a graduate student in
the Department of Nutrition and Exercise
Physiology at the University of Missouri
and the graduate assistant at Optimus:
The Center for Health.
Thomas P. LaFontaine is a clinical
exercise physiologist and personal health
and fitness mentor at Optimus: The Center
for Health.
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