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Parkinson's Disease: Epidemiology, Pathophysiology, and Exercise Intervention

Bollinger, Lance M. MA1; Cowan, Celsi E. BS2; LaFontaine, Thomas P. PhD3

Section Editor(s): Ronai, Peter MS, RCEP, CSCS*D, NSCA-CPT

Strength and Conditioning Journal: April 2012 - Volume 34 - Issue 2 - p 50–54
doi: 10.1519/SSC.0b013e3182441afd


1Kinesiology Department, East Carolina University, Greenville, North Carolina

2Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri

3University of Missouri, Columbia, Missouri



The Special Populations Column provides personal trainers who work with apparently healthy or medically cleared special populations with scientifically supported background information.


Lance M. Bollingeris pursuing a PhD in Bioenergetics and Exercise Science at East Carolina University.

Celsi E. Cowanis 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. LaFontaineis a clinical exercise physiologist and personal health and fitness mentor at Optimus: The Center for Health.

Parkinson's disease (PD) is a relatively common neurodegenerative 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 appears to be the leading risk factor for developing PD.

Common clinical symptoms of PD include tremors, bradykinesis (slow speed of movement), rigidity, and impaired postural reflexes (14,19). This is typically because of decreased or altered neurotransmission. Although PD is a progressive, degenerative neurological disease, evidence suggests that exercise intervention may help improve strength, balance, gait, and overall functional status. The aim of this article is to discuss the epidemiology, pathophysiology, and exercise considerations for persons with PD. Specific exercise recommendations are addressed in the accompanying One-on-One column.

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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 consciousness, and antidepressant 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 developing 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 mitochondrial dysfunction and/or reactive oxygen species formation (15). Interestingly, many of the dysregulated genes involved in the development of PD are also involved in mitochondrial regulation (15).

The 4 principal symptoms of PD are resting tremor, bradykinesis, rigidity, and decreased postural reflexes. Secondary motor symptoms include shuffling gait, festination, freezing, dystonia, hypomimia, dysarthria, dysphagia, sialorrhea, micrographia, and glabellar reflex. The definitions associated with Parkinson's disease are listed below:

  • Akathisia—restless sensation of lower extremities (also known as restless leg syndrome).
  • Cachexia—extreme weight loss, especially of skeletal muscles.
  • Dysarthria—poor articulation.
  • Dyskinesis—irregular movement patterns due to difficulty performing voluntary muscle contractions.
  • Dysphagia—difficulty swallowing.
  • Dystonia—abnormal tonicity of muscle tissues resulting in unnatural positions on head and/or limbs.
  • Festination—short rapid steps, usually in an attempt to maintain balance due to excess trunk flexion.
  • Freezing (motor block)—involuntary sudden loss of or inability to initiate movement.
  • Glabellar reflex—persistent blinking in response to repetitive tapping on forehead.
  • Hypomimia—reduced or loss of facial expressions.
  • Micrographia—progressively smaller handwriting.
  • Sialorrhea—excessive salivation.

Additionally, PD patients often suffer from nonmotor symptoms such as neuropsychiatric, cognitive impairment, autonomic, sensory, and sleep disorders. Both motor and nonmotor symptoms can present significant functional limitations that worsen with disease stage. Common symptoms and related functional limitations of PD can be found in Table 1. It should also be noted that PD may be accompanied by other age-associated conditions, such as hypertension, cardiovascular disease, and/or arthritis.

Table 1

Table 1

Often the initial symptoms are relatively minor and may be disregarded as due to aging. This can delay a correct diagnosis by as much as 2–3 years (16). Additionally, because PD is a progressive disease, diagnosis is not sufficient to indicate severity of disease. Several tools have been proposed to classify the stage of the disease. Perhaps, the most common tool used is the Hoehn and Yahr Staging Scale (13) (Table 2). Although these tools involve some degree of subjectivity, they can be very useful in determining functional status of the patient and provide some information as to progression of the disease.

Table 2

Table 2

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Although PD affects numerous areas of the central nervous system, the primary brain areas affected are the basal ganglia, 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 neurotransmitters such that dopamine is decreased, causing a relative increase in acetylcholine. The altered neurotransmitter 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 prescribed 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 oxidase-B, and catechol-O-methyl transferase inhibitors. These drugs function to decrease acetylcholine, slow the degradation of dopamine, and slow the degradation of L-DOPA, respectively. Common medications used in the treatment of PD can be found in Table 3.

Table 3

Table 3

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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 techniques is a function of the symptoms of the individual, functional limitations, and stage of disease. During early stages of PD (stages 1–2 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. Additionally, emphasizing functional training and motor control can improve balance, coordination, performance of ADLs, and independence.

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Flexibility training can effectively increase ROM and reduce rigidity. Rigidity, involuntary muscular resistance 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.

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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 1–3) (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 traditional 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.

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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 1–3) and healthy age-matched controls (21). This suggests PD does not inherently limit aerobic capacity. It is important to consider functional limitations 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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Functional training, such as balance and gait exercises, may improve the ability to perform ADLs. Compared with controls, persons with PD participating in physical therapy emphasizing functional training were significantly better able to perform ADLs (9). Balance exercise has been shown to improve both sensory orientation 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.

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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 improving independence. Exercise professionals should obtain medical clearance and maintain open communication with other members of the client's medical team. Additionally, being aware of the challenges presented by PD and being familiar with strategies to effectively implement exercise may improve quality of life for PD patients.

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